Potassium Cyanide
Cyanides
Potassium
Chemoreceptor Cells
Sodium Azide
Hydrogen Cyanide
Oxygen Consumption
Oxidation-Reduction
Potassium Channels
Sodium Cyanide
Electron Transport
Adenosine Triphosphate
Hydrogen-Ion Concentration
Hydrogen Peroxide
Organic cation transport in rat choroid plexus cells studied by fluorescence microscopy. (1/405)
Quinacrine uptake and distribution were studied in a primary culture of rat choroid plexus epithelial cells using conventional and confocal fluorescence microscopy and image analysis. Quinacrine rapidly accumulated in cells, with steady-state levels being achieved after 10-20 min. Uptake was reduced by other organic cations, e.g., tetraethylammonium (TEA), and by KCN. Quinacrine fluorescence was distributed in two cytoplasmic compartments, one diffuse and the other punctate. TEA efflux experiments indicated that more than one-half of intracellular organic cation was in a slowly emptying compartment. The protonophore monensin both emptied that TEA compartment and abolished punctate quinacrine fluorescence, suggesting that a large fraction of total intracellular organic cation was sequestered in acidic vesicles, e.g., endosomes. Finally, quinacrine-loaded vesicles were seen to move within the cytoplasm and to abruptly release their contents at the blood side of the cell; the rate of release was greatly reduced by the microtubule disrupter nocodazole. (+info)Arterial chemoreflex in conscious normotensive and hypertensive adult rats. (2/405)
Evidence from human and animal studies suggests that the arterial chemoreflex may be exaggerated in essential hypertension. In the present study, cardiorespiratory responses to peripheral chemoreceptor stimulation were compared in conscious unrestrained spontaneously hypertensive (SH) and normotensive Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats (13-14 wk old). Chemoreceptors were stimulated by injections of potassium cyanide (30-125 microgram/kg iv). Chemoreceptor stimulation elicited a pressor response and bradycardia. The peak change in mean arterial pressure evoked during chemoreceptor stimulation was not significantly different between SH (n = 18) and WKY (n = 18) rats but was significantly smaller in SD rats (n = 18). An evaluation of respiratory responses to chemoreceptor stimulation in conscious and anesthetized rats also demonstrated no significant difference between SH and WKY rats, but the response of the SD rats tended to be smaller. These results demonstrate that differences in the arterial chemoreflex response of SH vs. normotensive rats are not linked to hypertension but, rather, to differences between rat strains. (+info)Oxygen sensing in yeast: evidence for the involvement of the respiratory chain in regulating the transcription of a subset of hypoxic genes. (3/405)
Oxygen availability affects the transcription of a number of genes in nearly all organisms. Although the molecular mechanisms for sensing oxygen are not precisely known, heme is thought to play a pivotal role. Here, we address the possibility that oxygen sensing in yeast, as in mammals, involves a redox-sensitive hemoprotein. We have found that carbon monoxide (CO) completely blocks the anoxia-induced expression of two hypoxic genes, OLE1 and CYC7, partially blocks the induction of a third gene, COX5b, and has no effect on the expression of other hypoxic or aerobic genes. In addition, transition metals (Co and Ni) induce the expression of OLE1 and CYC7 in a concentration-dependent manner under aerobic conditions. These findings suggest that the redox state of an oxygen-binding hemoprotein is involved in controlling the expression of at least two hypoxic yeast genes. By using mutants deficient in each of the two major yeast CO-binding hemoproteins (cytochrome c oxidase and flavohemoglobin), respiratory inhibitors, and cob1 and rho0 mutants, we have found that the respiratory chain is involved in the anoxic induction of these two genes and that cytochrome c oxidase is likely the hemoprotein "sensor." Our findings also indicate that there are at least two classes of hypoxic genes in yeast (CO sensitive and CO insensitive) and imply that multiple pathways/mechanisms are involved in modulating the expression of hypoxic yeast genes. (+info)Calcium antagonists ameliorate ischemia-induced endothelial cell permeability by inhibiting protein kinase C. (4/405)
BACKGROUND: Dihydropyridines block calcium channels; however, they also influence endothelial cells, which do not express calcium channels. We tested the hypothesis that nifedipine can prevent ischemia-induced endothelial permeability increases by inhibiting protein kinase C (PKC) in cultured porcine endothelial cells. METHODS AND RESULTS: Ischemia was induced by potassium cyanide/deoxyglucose, and permeability was measured by albumin flux. Ion channels were characterized by patch clamp. [Ca2+]i was measured by fura 2. PKC activity was measured by substrate phosphorylation after cell fractionation. PKC isoforms were assessed by Western blot and confocal microscopy. Nifedipine prevented the ischemia-induced increase in permeability in a dose-dependent manner. Ischemia increased [Ca2+]i, which was not affected by nifedipine. Instead, ischemia-induced PKC translocation was prevented by nifedipine. Phorbol ester also increased endothelial cell permeability, which was dose dependently inhibited by nifedipine. The effects of non-calcium-channel-binding dihydropyridine derivatives were similar. Analysis of the PKC isoforms showed that nifedipine prevented ischemia-induced translocation of PKC-alpha and PKC-zeta. Specific inhibition of PKC isoforms with antisense oligodeoxynucleotides demonstrated a major role for PKC-alpha. CONCLUSIONS: Nifedipine exerts a direct effect on endothelial cell permeability that is independent of calcium channels. The inhibition of ischemia-induced permeability by nifedipine seems to be mediated primarily by PKC-alpha inhibition. Anti-ischemic effects of dihydropyridine calcium antagonists could be due in part to their effects on endothelial cell permeability. (+info)Diffusion of dialkylnitrosamines into the rat esophagus as a factor in esophageal carcinogenesis. (5/405)
To indicate how readily nitrosamines (NAms) diffuse into the esophagus, we measured diffusion rate (flux) through rat esophagus of dialkyl-NAms using side-by-side diffusion apparatuses. Mucosal and serosal flux at 37 degrees C of two NAms, each at 50 microM, was followed for 90 min by gas chromatography-thermal energy analysis of NAms in the receiver chamber. Mucosal flux of one or two NAms at a time gave identical results. Mucosal flux was highest for the strong esophageal carcinogens methyl-n-amyl-NAm (MNAN) and methylbenzyl-NAm. Mucosal esophageal flux of 11 NAms was 18-280 times faster and flux of two NAms through skin was 13-28 times faster than that predicted for skin from the molecular weights and octanol:water partition coefficients, which were also measured. Mucosal: serosal flux ratio was correlated (P < 0.05) with esophageal carcinogenicity and molecular weight. For seven NAms tested for carcinogenicity by Druckrey et al. [(1967) Z. Krebsforsch., 69, 103-201], mucosal flux was correlated with esophageal carcinogenicity with borderline significance (P = 0.07). The MNAN:dipropyl-NAm ratio for mucosal esophageal flux was unaffected when rats were treated with phenethylisothiocyanate and was similar to that for forestomach, indicating no involvement by cytochromes P450. Mucosal esophageal flux of MNAN and dimethyl-NAm was reduced by >90% on enzymic removal of the stratum corneum, was unaffected by 0.1 mM verapamil and was inhibited 67-94% by 1.0 mM KCN and 82-93% by 0.23% ethanol. NAm flux through rat skin and jejunum was 5-17% of that through esophagus. Flux through skin increased 5-13 times after enzymic or mechanical removal of the epidermis; the histology probably explained this difference from esophagus. Hence, NAms could be quite rapidly absorbed by human esophagus when NAm-containing foods or beverages are swallowed, the esophageal carcinogenicity of NAms may be partly determined by their esophageal flux and NAm flux probably occurs by passive diffusion. (+info)The plasma membrane NADH oxidase of HeLa cells has hydroquinone oxidase activity. (6/405)
The plasma membrane NADH oxidase activity partially purified from the surface of HeLa cells exhibited hydroquinone oxidase activity. The preparations completely lacked NADH:ubiquinone reductase activity. However, in the absence of NADH, reduced coenzyme Q10 (Q10H2=ubiquinol) was oxidized at a rate of 15+/-6 nmol min-1 mg protein-1 depending on degree of purification. The apparent Km for Q10H2 oxidation was 33 microM. Activities were inhibited competitively by the cancer cell-specific NADH oxidase inhibitors, capsaicin and the antitumor sulfonylurea N-(4-methylphenylsulfonyl)-N'-(4-chlorophenyl)urea (LY181984). With coenzyme Q0, where the preparations were unable to carry out either NADH:quinone reduction or reduced quinone oxidation, quinol oxidation was observed with an equal mixture of the Q0 and Q0H2 forms. With the mixture, a rate of Q0H2 oxidation of 8-17 nmol min-1 mg protein-1 was observed with an apparent Km of 0.22 mM. The rate of Q10H2 oxidation was not stimulated by addition of equal amounts of Q10 and Q10H2. However, addition of Q0 to the Q10H2 did stimulate. The oxidation of Q10H2 proceeded with what appeared to be a two-electron transfer. The oxidation of Q0H2 may involve Q0, but the mechanism was not clear. The findings suggest the potential participation of the plasma membrane NADH oxidase as a terminal oxidase of plasma membrane electron transport from cytosolic NAD(P)H via naturally occurring hydroquinones to acceptors at the cell surface. (+info)Calcium-dependent PAF-stimulated generation of reactive oxygen species in a human keratinocyte cell line. (7/405)
During inflammation and other pathological states, the lipid mediator platelet-activating factor (PAF) and reactive oxygen species (ROS) are both generated. We have been investigating the effect of exogenous PAF on ROS formation in the human keratinocyte cell line (HaCaT). ROS production, measured using luminol-enhanced chemiluminescence (CL), proved to be rapid, transient, PAF receptor-mediated, and totally dependent on an increase in intracellular Ca2+ ([Ca2+]i) and on the presence of extracellular Ca2+. Repeated administration of PAF resulted in refractoriness to the agonist in terms of both capacities to increase [Ca2+]i and generate ROS. The cells, however, continued to respond fully to other stimulants (bradykinin, epidermal growth factor, thapsigargin). The PAF-induced increases in [Ca2+]i (monitored using the fluorescent probe Fluo-3) were also rapid and transient and paralleled those of ROS generation. Relatively specific inhibitors of potential ROS-producing systems were administered in an attempt to characterize the ROS producing system(s). Inhibitors of xanthine oxidase, phospholipase A2, lipoxygenase, cyclooxygenase and NO synthase did not interfere with PAF evoked ROS. The flavoprotein inhibitor diphenyleneiodonium and the mitochondrial cytochrome oxidase inhibitor KCN, prevented generation of ROS, making NAD(P)H a candidate for the electron source of the ROS and the mitochondria a potential major site of formation. (+info)BDNF attenuates retinal cell death caused by chemically induced hypoxia in rats. (8/405)
PURPOSE: To investigate the neuroprotective effects of brain-derived neurotrophic factor (BDNF) against potassium cyanide (KCN)-induced retinal damage. METHODS: Rats were injected intravitreally with iodinated BDNF. Two days later, eyeballs were dissected into various parts, and the level of radioactivity in each part was measured. Retinal damage was induced by incubating rat eyeballs with 5 mM KCN. BDNF was injected intravitreally 2 days before KCN treatment, and subsequent morphometric analysis was carried out to evaluate the retinal cell damage. To elucidate the mechanisms of BDNF's neuroprotective effects, the intravitreal concentrations of amino acids and the expression of calretinin were investigated. RESULTS: Intravitreally injected BDNF was distributed evenly throughout the eyes, and the incorporation of iodinated BDNF into the retina was three times higher than in other ocular tissues. Immunohistochemical analysis demonstrated that exogenous BDNF diffused throughout the retina and was especially concentrated in the inner (INL) and outer nuclear layer. Morphometric analysis showed that the number of INL cells of the posterior area, 880 microm from the optic nerve head, was 190 +/- 4 with KCN treatment and 284 +/- 9 in control animals. Cell death appeared to be necrotic. When eyes injected with either phosphate-buffered saline (PBS) or BDNF were subjected to treatment with KCN, the number of INL cells was 186 +/- 5 in the PBS-treated controls and 253 +/- 8 in eyes treated with BDNF. Also, BDNF increased the number of calretinin-positive cells in the INL and reduced the KCN-induced elevation of intravitreal glutamate levels. CONCLUSIONS: BDNF injected intravitreally reaches the retina and attenuates the INL cell death caused by KCN-induced metabolic insult. The neuroprotective effects of BDNF are partly ascribed to the upregulation of a calcium-binding protein and the attenuation of glutamate release into the vitreous body. (+info)Potassium Cyanide (C6H5KN) is defined as a white, water-soluble, crystalline salt that is highly toxic. It is used in fumigation, electroplating, and metal cleaning. When combined with acids, it releases the deadly gas hydrogen cyanide. It can cause immediate death by inhibiting cellular respiration. It is also known as Cyanide of Potassium or Potassium Salt of Hydrocyanic Acid.
Cyanides are a group of chemical compounds that contain the cyano group, -CN, which consists of a carbon atom triple-bonded to a nitrogen atom. They are highly toxic and can cause rapid death due to the inhibition of cellular respiration. Cyanide ions (CN-) bind to the ferric iron in cytochrome c oxidase, a crucial enzyme in the electron transport chain, preventing the flow of electrons and the production of ATP, leading to cellular asphyxiation.
Common sources of cyanides include industrial chemicals such as hydrogen cyanide (HCN) and potassium cyanide (KCN), as well as natural sources like certain fruits, nuts, and plants. Exposure to high levels of cyanides can occur through inhalation, ingestion, or skin absorption, leading to symptoms such as headache, dizziness, nausea, vomiting, rapid heartbeat, seizures, coma, and ultimately death. Treatment for cyanide poisoning typically involves the use of antidotes that bind to cyanide ions and convert them into less toxic forms, such as thiosulfate and rhodanese.
Potassium is a essential mineral and an important electrolyte that is widely distributed in the human body. The majority of potassium in the body (approximately 98%) is found within cells, with the remaining 2% present in blood serum and other bodily fluids. Potassium plays a crucial role in various physiological processes, including:
1. Regulation of fluid balance and maintenance of normal blood pressure through its effects on vascular tone and sodium excretion.
2. Facilitation of nerve impulse transmission and muscle contraction by participating in the generation and propagation of action potentials.
3. Protein synthesis, enzyme activation, and glycogen metabolism.
4. Regulation of acid-base balance through its role in buffering systems.
The normal serum potassium concentration ranges from 3.5 to 5.0 mEq/L (milliequivalents per liter) or mmol/L (millimoles per liter). Potassium levels outside this range can have significant clinical consequences, with both hypokalemia (low potassium levels) and hyperkalemia (high potassium levels) potentially leading to serious complications such as cardiac arrhythmias, muscle weakness, and respiratory failure.
Potassium is primarily obtained through the diet, with rich sources including fruits (e.g., bananas, oranges, and apricots), vegetables (e.g., leafy greens, potatoes, and tomatoes), legumes, nuts, dairy products, and meat. In cases of deficiency or increased needs, potassium supplements may be recommended under the guidance of a healthcare professional.
Chemoreceptor cells are specialized sensory neurons that detect and respond to chemical changes in the internal or external environment. They play a crucial role in maintaining homeostasis within the body by converting chemical signals into electrical impulses, which are then transmitted to the central nervous system for further processing and response.
There are two main types of chemoreceptor cells:
1. Oxygen Chemoreceptors: These cells are located in the carotid bodies near the bifurcation of the common carotid artery and in the aortic bodies close to the aortic arch. They monitor the levels of oxygen, carbon dioxide, and pH in the blood and respond to decreases in oxygen concentration or increases in carbon dioxide and hydrogen ions (indicating acidity) by increasing their firing rate. This signals the brain to increase respiratory rate and depth, thereby restoring normal oxygen levels.
2. Taste Cells: These chemoreceptor cells are found within the taste buds of the tongue and other areas of the oral cavity. They detect specific tastes (salty, sour, sweet, bitter, and umami) by interacting with molecules from food. When a tastant binds to receptors on the surface of a taste cell, it triggers a series of intracellular signaling events that ultimately lead to the generation of an action potential. This information is then relayed to the brain, where it is interpreted as taste sensation.
In summary, chemoreceptor cells are essential for maintaining physiological balance by detecting and responding to chemical stimuli in the body. They play a critical role in regulating vital functions such as respiration and digestion.
Sodium azide is a chemical compound with the formula NaN3. Medically, it is not used as a treatment, but it can be found in some pharmaceutical and laboratory settings. It is a white crystalline powder that is highly soluble in water and has a relatively low melting point.
Sodium azide is well known for its ability to release nitrogen gas upon decomposition, which makes it useful as a propellant in airbags and as a preservative in laboratory settings to prevent bacterial growth. However, this property also makes it highly toxic to both animals and humans if ingested or inhaled, as it can cause rapid respiratory failure due to the release of nitrogen gas in the body. Therefore, it should be handled with great care and appropriate safety measures.
Hydrogen Cyanide (HCN) is a chemical compound with the formula H-C≡N. It is a colorless, extremely poisonous and flammable liquid that has a bitter almond-like odor in its pure form. However, not everyone can detect its odor, as some people lack the ability to smell it, which makes it even more dangerous. It is soluble in water and alcohol, and its aqueous solution is called hydrocyanic acid or prussic acid.
Hydrogen Cyanide is rapidly absorbed by inhalation, ingestion, or skin contact, and it inhibits the enzyme cytochrome c oxidase, which is essential for cellular respiration. This leads to rapid death due to hypoxia (lack of oxygen) at the cellular level. It is used industrially in large quantities as a pesticide, fumigant, and chemical intermediate, but it also has significant potential for use as a chemical weapon.
In the medical field, Hydrogen Cyanide poisoning can be treated with high-concentration oxygen, sodium nitrite, and sodium thiosulfate, which help to restore the function of cytochrome c oxidase and enhance the elimination of cyanide from the body.
Dinitrophenols (DNP) are a class of chemical compounds that contain two nitro groups (-NO2) attached to a phenol group. Dinitrophenols have been used in the past as industrial dyes, wood preservatives, and pesticides. However, they have also been misused as weight loss supplements due to their ability to increase metabolic rate and cause weight loss.
The use of DNP for weight loss is dangerous and has been linked to several fatalities. DNP works by disrupting the normal functioning of the mitochondria in cells, which are responsible for producing energy. This disruption causes an increase in metabolic rate, leading to a rapid breakdown of fat and carbohydrates, and ultimately weight loss. However, this increased metabolism can also produce excessive heat, leading to hyperthermia, dehydration, and damage to organs such as the heart, liver, and kidneys.
Due to their potential for serious harm, DNP-containing products are banned in many countries, including the United States. Medical professionals should be aware of the dangers associated with DNP use and advise patients accordingly.
Oxygen consumption, also known as oxygen uptake, is the amount of oxygen that is consumed or utilized by the body during a specific period of time, usually measured in liters per minute (L/min). It is a common measurement used in exercise physiology and critical care medicine to assess an individual's aerobic metabolism and overall health status.
In clinical settings, oxygen consumption is often measured during cardiopulmonary exercise testing (CPET) to evaluate cardiovascular function, pulmonary function, and exercise capacity in patients with various medical conditions such as heart failure, chronic obstructive pulmonary disease (COPD), and other respiratory or cardiac disorders.
During exercise, oxygen is consumed by the muscles to generate energy through a process called oxidative phosphorylation. The amount of oxygen consumed during exercise can provide important information about an individual's fitness level, exercise capacity, and overall health status. Additionally, measuring oxygen consumption can help healthcare providers assess the effectiveness of treatments and rehabilitation programs in patients with various medical conditions.
Oxidation-Reduction (redox) reactions are a type of chemical reaction involving a transfer of electrons between two species. The substance that loses electrons in the reaction is oxidized, and the substance that gains electrons is reduced. Oxidation and reduction always occur together in a redox reaction, hence the term "oxidation-reduction."
In biological systems, redox reactions play a crucial role in many cellular processes, including energy production, metabolism, and signaling. The transfer of electrons in these reactions is often facilitated by specialized molecules called electron carriers, such as nicotinamide adenine dinucleotide (NAD+/NADH) and flavin adenine dinucleotide (FAD/FADH2).
The oxidation state of an element in a compound is a measure of the number of electrons that have been gained or lost relative to its neutral state. In redox reactions, the oxidation state of one or more elements changes as they gain or lose electrons. The substance that is oxidized has a higher oxidation state, while the substance that is reduced has a lower oxidation state.
Overall, oxidation-reduction reactions are fundamental to the functioning of living organisms and are involved in many important biological processes.
Potassium channels are membrane proteins that play a crucial role in regulating the electrical excitability of cells, including cardiac, neuronal, and muscle cells. These channels facilitate the selective passage of potassium ions (K+) across the cell membrane, maintaining the resting membrane potential and shaping action potentials. They are composed of four or six subunits that assemble to form a central pore through which potassium ions move down their electrochemical gradient. Potassium channels can be modulated by various factors such as voltage, ligands, mechanical stimuli, or temperature, allowing cells to fine-tune their electrical properties and respond to different physiological demands. Dysfunction of potassium channels has been implicated in several diseases, including cardiac arrhythmias, epilepsy, and neurodegenerative disorders.
Sodium cyanide is a highly toxic chemical compound with the formula NaCN. It is a white solid that is readily soluble in water, and it has a bitter, almond-like odor that some people can detect. Sodium cyanide is used in various industrial processes, including metal cleaning and electroplating, but it is perhaps best known as a poison.
Cyanide ions (CN-) are extremely toxic because they bind to the ferric iron (Fe3+) in cytochrome c oxidase, a crucial enzyme in the mitochondria that is responsible for cellular respiration and energy production. When cyanide ions bind to this enzyme, it becomes unable to function, leading to a rapid depletion of ATP (adenosine triphosphate) and an accumulation of lactic acid, which can cause metabolic acidosis, coma, and death within minutes to hours.
It is important to note that sodium cyanide should be handled with extreme care and only by trained professionals who are familiar with its hazards and proper safety protocols. Exposure to this compound can cause severe health effects, including respiratory failure, convulsions, and cardiac arrest.
The Electron Transport Chain (ETC) is a series of complexes in the inner mitochondrial membrane that are involved in the process of cellular respiration. It is the final pathway for electrons derived from the oxidation of nutrients such as glucose, fatty acids, and amino acids to be transferred to molecular oxygen. This transfer of electrons drives the generation of a proton gradient across the inner mitochondrial membrane, which is then used by ATP synthase to produce ATP, the main energy currency of the cell.
The electron transport chain consists of four complexes (I-IV) and two mobile electron carriers (ubiquinone and cytochrome c). Electrons from NADH and FADH2 are transferred to Complex I and Complex II respectively, which then pass them along to ubiquinone. Ubiquinone then transfers the electrons to Complex III, which passes them on to cytochrome c. Finally, cytochrome c transfers the electrons to Complex IV, where they combine with oxygen and protons to form water.
The transfer of electrons through the ETC is accompanied by the pumping of protons from the mitochondrial matrix to the intermembrane space, creating a proton gradient. The flow of protons back across the inner membrane through ATP synthase drives the synthesis of ATP from ADP and inorganic phosphate.
Overall, the electron transport chain is a crucial process for generating energy in the form of ATP in the cell, and it plays a key role in many metabolic pathways.
Adenosine Triphosphate (ATP) is a high-energy molecule that stores and transports energy within cells. It is the main source of energy for most cellular processes, including muscle contraction, nerve impulse transmission, and protein synthesis. ATP is composed of a base (adenine), a sugar (ribose), and three phosphate groups. The bonds between these phosphate groups contain a significant amount of energy, which can be released when the bond between the second and third phosphate group is broken, resulting in the formation of adenosine diphosphate (ADP) and inorganic phosphate. This process is known as hydrolysis and can be catalyzed by various enzymes to drive a wide range of cellular functions. ATP can also be regenerated from ADP through various metabolic pathways, such as oxidative phosphorylation or substrate-level phosphorylation, allowing for the continuous supply of energy to cells.
Hydrogen-ion concentration, also known as pH, is a measure of the acidity or basicity of a solution. It is defined as the negative logarithm (to the base 10) of the hydrogen ion activity in a solution. The standard unit of measurement is the pH unit. A pH of 7 is neutral, less than 7 is acidic, and greater than 7 is basic.
In medical terms, hydrogen-ion concentration is important for maintaining homeostasis within the body. For example, in the stomach, a high hydrogen-ion concentration (low pH) is necessary for the digestion of food. However, in other parts of the body such as blood, a high hydrogen-ion concentration can be harmful and lead to acidosis. Conversely, a low hydrogen-ion concentration (high pH) in the blood can lead to alkalosis. Both acidosis and alkalosis can have serious consequences on various organ systems if not corrected.
Hydrogen peroxide (H2O2) is a colorless, odorless, clear liquid with a slightly sweet taste, although drinking it is harmful and can cause poisoning. It is a weak oxidizing agent and is used as an antiseptic and a bleaching agent. In diluted form, it is used to disinfect wounds and kill bacteria and viruses on the skin; in higher concentrations, it can be used to bleach hair or remove stains from clothing. It is also used as a propellant in rocketry and in certain industrial processes. Chemically, hydrogen peroxide is composed of two hydrogen atoms and two oxygen atoms, and it is structurally similar to water (H2O), with an extra oxygen atom. This gives it its oxidizing properties, as the additional oxygen can be released and used to react with other substances.
In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."
1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.
2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.
3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.
4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).
Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.
Temperature, in a medical context, is a measure of the degree of hotness or coldness of a body or environment. It is usually measured using a thermometer and reported in degrees Celsius (°C), degrees Fahrenheit (°F), or kelvin (K). In the human body, normal core temperature ranges from about 36.5-37.5°C (97.7-99.5°F) when measured rectally, and can vary slightly depending on factors such as time of day, physical activity, and menstrual cycle. Elevated body temperature is a common sign of infection or inflammation, while abnormally low body temperature can indicate hypothermia or other medical conditions.
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Sodium cyanide and potassium cyanide3
- Hydrogen cyanide (HCN), which is a gas, and the simple cyanide salts (sodium cyanide and potassium cyanide) are common examples of cyanide compounds. (cdc.gov)
- Hydrogen cyanide, sodium cyanide, and potassium cyanide are the forms of cyanide most likely to be in the environment as a result of industrial activities. (cdc.gov)
- Sodium cyanide and potassium cyanide are both white solids with a slight, bitter, almond-like odor in damp air. (cdc.gov)
Doses of potassium cyanide1
- Someone had opened the capsules and replaced the pain-relieving medicine with deadly doses of potassium cyanide. (history.com)
Grams of potassium cyanide2
- Evidence presented during the trial indicated that Ghane unlawfully possessed 177 grams of potassium cyanide, a highly toxic chemical that is fatal in even small doses, which he stole from the chemistry laboratory at Maple Woods Community College. (justice.gov)
- For some inexplicable reason, Kilmartin didn't part with any of his 100 grams of potassium cyanide, he sent Andrew a gram of Epsom Salts. (annaraccoon.com)
Effects of potassium cyanide3
- The effects of potassium cyanide and sodium cyanide are identical, and symptoms of poisoning typically occur within a few minutes of ingesting the substance: the person loses consciousness, and brain death eventually follows. (wikipedia.org)
- One way that can help counter the effects of potassium cyanide is taking a significant amount of glucose. (healthontimeus.com)
- What are the side effects of potassium cyanide? (healthontimeus.com)
Body's ability to use oxygen2
- Potassium cyanide releases hydrogen cyanide gas, a highly toxic chemical asphyxiant that interferes with the body's ability to use oxygen. (cdc.gov)
- A highly toxic product works by releasing hydrogen cyanide gas that is highly toxic as well and cuts your body's ability to use oxygen. (healthontimeus.com)
POWDER3
- For aqueous solutions of cyanide, apply excess FAST-ACT powder. (fast-act.com)
- People mostly ship potassium cyanide in tablets, or powder form. (healthontimeus.com)
- If you are shipping from us, the available dosages are a 10mg oral tablet or potassium cyanide powder. (healthontimeus.com)
Salts5
- Much smaller amounts of cyanide may enter water through storm water runoff where road salts are used that contain cyanide. (cdc.gov)
- Four incidents of cyanide in soil resulted from disposal of cyanide-containing wastes in landfills and use of cyanide-containing road salts. (cdc.gov)
- There are many possible reasons for high use of cyanide salts. (finishing.com)
- What's a man to do when the FBI hold irrefutable evidence that he had advertised potassium cyanide but only sent Epsom Salts? (annaraccoon.com)
- The concept is distinguished from CYANIDES, which denotes inorganic salts of HYDROGEN CYANIDE. (bvsalud.org)
Hydrogen cya1
- The hydrogen cyanide gas has a unique bitter almond odor. (healthontimeus.com)
Alkali Metal Cyanides2
- Before 1900 and the invention of the Castner process, potassium cyanide was the most important source of alkali metal cyanides. (wikipedia.org)
- The alkali-metal cyanides and strong acids dissolve it quickly. (abbaworld.com)
NaCN1
- KCN and sodium cyanide (NaCN) are widely used in organic synthesis for the preparation of nitriles and carboxylic acids, particularly in the von Richter reaction. (wikipedia.org)
Toxic5
- Potassium cyanide is highly toxic, and a dose of 200 to 300 milligrams will kill nearly any human. (wikipedia.org)
- As said above, potassium cyanide is very toxic and poisonous just like sodium cyanide. (healthontimeus.com)
- Hydrogen cyanide is a toxic gas that may enter the environment from both natural processes and human industrial activities. (cdc.gov)
- Also, there are many different types of cyanide (potassium, hydrogen, sodium), most or all of which are toxic and should not be consumed in large amounts. (todayifoundout.com)
- This will reduce reliance on the HiCN method which uses toxic potassium cyanide. (euramet.org)
Ferricyanide2
- One example of such complex formation is the reaction of cyanide with iron in the formation of ferrocyanide and ferricyanide complexes. (cdc.gov)
- The principle of this method is based on the conversion of hemoglobin to cyanmethemoglobin by the addition of potassium cyanide and ferricyanide whose absorbance is measured at 540 nm in a colorimeter or spectrophotometer against a standard solution. (who.int)
Hydroxide2
- KCN is produced by treating hydrogen cyanide with an aqueous solution of potassium hydroxide, followed by evaporation of the solution in a vacuum: HCN + KOH → KCN + H2O About 50,000 tons of potassium cyanide are produced yearly. (wikipedia.org)
- When an alkyl halide containing a beta-hydrogen is heated with a solution containing alcoholic potassium hydroxide, a hydrogen atom is eliminated from beta-carbon, an atom of halogen is eliminated from alpha-carbon and an alkene is obtained. (bartleby.com)
Contain cyanide1
- Several more bottles in the Chicago area were found to contain cyanide, but thankfully no one else was hurt. (history.com)
Inorganic2
- Potassium cyanide is a very poisonous inorganic cyanide salt, which people can use instead of the more popular sodium cyanide. (healthontimeus.com)
- view phone in south Africa pretoria , Johannesburg cape town , Durban , rastenburg providing a fine range of Chemicals such as Acids, Caustic ills in this sector, we have been successfully engaged in manufacturing and supplying potassium Cyanide, which is an inorganic compound with the formula Kcn. (drjamesguerrero.com)
Chemical8
- Such solutions should be kept alkaline whenever possible so as to eliminate the possibility of generation of hydrogen cyanide: KCN + H2O2 → KOCN + H2O KCN + NaOCl → KOCN + NaCl NIOSH Pocket Guide to Chemical Hazards. (wikipedia.org)
- Potassium cyanide is the chemical of choice in surface treatment, electroplating and gilding. (draslovka.com)
- Potassium cyanide is more reactive than the alternative sodium cyanide, a quality beneficial in pharmaceutical intermediates and chemical specialities use. (draslovka.com)
- Cyanide is a chemical group consisting of one atom of carbon connected to one atom of nitrogen by three molecular bonds (C≡N) and cyanides are compounds (substances formed by the joining of two or more atoms) that contain a cyanide group (typically shown as CN). (cdc.gov)
- The major sources of cyanides in water are discharges from some metal mining processes, organic chemical industries, iron and steel plants or manufacturers, and publicly owned wastewater treatment facilities. (cdc.gov)
- Other cyanide sources include vehicle exhaust, releases from certain chemical industries, burning of municipal waste, and use of cyanide-containing pesticides. (cdc.gov)
- Information regarding the chemical identity of the most common cyanides is located in Table 4-1. (cdc.gov)
- Information regarding the physical and chemical properties of cyanide is located in Table 4-2. (cdc.gov)
Cyanogen chloride2
Ramcharitmanas1
- Bihar's Education Minister, Chandra Shekhar, has sparked controversy by likening elements in ancient scriptures like the Ramcharitmanas to "potassium cyanide. (odishabhaskar.in)
Inhibitor3
- Potassium cyanide is a potent inhibitor of cellular respiration, acting on mitochondrial cytochrome c oxidase, hence blocking oxidative phosphorylation. (wikipedia.org)
- Potassium cyanide is a highly poisonous compound that is an inhibitor of many metabolic processes, but has been shown to be an especially potent inhibitor of heme enzymes and haemoproteins. (bestchemplug.com)
- To determine whether this bridging sulfide is catalytically relevant and to further explore the mechanism of the C-cluster, we obtained crystal structures of the 310 kDa bifunctional CODH/acetyl-CoA synthase complex from Moorella thermoacetica bound both with a substrate H(2)O/OH(-) molecule and with a cyanide inhibitor. (rcsb.org)
Odor3
- Hydrogen cyanide is often described a having an odor resembling that of bitter almonds. (wikipedia.org)
- Hydrogen cyanide is a colorless gas with a faint, bitter, almond-like odor. (cdc.gov)
- On our first morning in Boston, we exited the Park Street Station en route to Boston Common but instead of being greeted by the aroma of molasses, we were hit full-on with a pungent repulsive odor. (medscape.com)
Chemicals2
- Buy Potassium Cyanide Online , If you are familiar with chemicals, you probably know about potassium cyanide. (healthontimeus.com)
- The park contained dangerous chemicals such as potassium cyanide, and there were many residents in the area. (chinadaily.com.cn)
Compounds4
- Potassium Cyanide (KCN), perhaps, is one of the most prevalent compounds known to humanity. (buycocainepill.com)
- In certain plant foods, including almonds, millet sprouts, lima beans, soy, spinach, bamboo shoots, and cassava roots (which are a major source of food in tropical countries), cyanides occur naturally as part of sugars or other naturally-occurring compounds. (cdc.gov)
- The cyanide compounds in which cyanide can be obtained as CN- are classified as simple and complex cyanides. (cdc.gov)
- Cyanogenic glycosides are cyanide compounds produced naturally in many plants (Jones 1998). (cdc.gov)
Compound1
- Potassium cyanide is a compound with the formula KCN. (wikipedia.org)
Ores2
- Potassium cyanide is used commercially for fumigation, electroplating, and extracting gold and silver from ores. (cdc.gov)
- Commercial uses of potassium cyanide are fumigation, extracting silver and gold from ores, and electroplating. (healthontimeus.com)
Fatal3
- Exposure to potassium cyanide can be rapidly fatal. (cdc.gov)
- Exposing yourself to potassium cyanide can be fatal. (healthontimeus.com)
- Andrew took himself off to a nearby hotel and drank what he thought was a fatal dose of cyanide. (annaraccoon.com)
Ions5
- In this historical process, potassium cyanide was produced by decomposing potassium ferrocyanide: K4[Fe(CN)6] → 4 KCN + FeC2 + N2 In aqueous solution, KCN is dissociated into hydrated potassium (K+) ions and cyanide (CN−) ions. (wikipedia.org)
- As a solid, KCN has structure resembling sodium chloride: with each potassium ion surrounded by six cyanide ions, and vice versa. (wikipedia.org)
- Despite being diatomic, and thus less symmetric than chloride, the cyanide ions rotate so rapidly that their time-averaged shape is spherical. (wikipedia.org)
- At low temperature and high pressure, this free rotation is hindered, resulting in a less symmetric crystal structure with the cyanide ions arranged in sheets. (wikipedia.org)
- Solutions of ferrocyanides and ferricyanides can form hydrogen cyanide and cyanide ions when exposed to sunlight or ultraviolet radiation. (cdc.gov)
Hydrolysis2
- The moist solid emits small amounts of hydrogen cyanide due to hydrolysis (reaction with water). (wikipedia.org)
- At neutral pH, cyanogen undergoes a slow hydrolysis to form hydrogen cyanide, cyanic acid (HOCN), and other products. (cdc.gov)
Amounts1
- However, the edible parts of plants that are eaten in the United States, including tapioca which is made from cassava roots, contain relatively low amounts of cyanide. (cdc.gov)
Methemoglobin1
- methemoglobin) and then converts it to hemoglobin cyanide (HiCN). (medscape.com)
Copper1
- and calcium cyanide, Ca(CN)2), while others are sparingly soluble or almost insoluble (copper (I) cyanide, CuCN). (cdc.gov)
Fumigation1
- The most common signs of potassium cyanide are extraction, electroplating, fumigation, and photographic development. (healthontimeus.com)
Bitter1
- The taste of potassium cyanide has been described as acrid and bitter, with a burning sensation[unreliable source? (wikipedia.org)
Contaminate3
- Water: Potassium cyanide can be used to contaminate water. (cdc.gov)
- Agricultural: If potassium cyanide is released as fine droplets, liquid spray (aerosol), or fine particles, it has the potential to contaminate agricultural products. (cdc.gov)
- Cyanide in landfills can contaminate underground water. (cdc.gov)
Oxygen1
- Initially, acute cyanide poisoning causes a red or ruddy complexion in the victim because the tissues are not able to use the oxygen in the blood. (wikipedia.org)
Consumption2
- The pill form of Potassium cyanide is highly concentrated and the consumption of an overdose leads to death. (healthontimeus.com)
- While acknowledging the positive aspects of the scriptures, the minister used an analogy, stating that just as a feast tainted with potassium cyanide becomes unfit for consumption, these scriptures have concerning elements. (odishabhaskar.in)
Acid1
- A. Is there a possibility that you are dragging in acid (which kills the cyanide) from your pretreatment? (finishing.com)
Acute1
- Acute disruption of cochlear potentials by potassium cyanide. (cdc.gov)
Glucose2
- Glucose binds to the cyanide fast, disconnecting it to bond with the cells. (healthontimeus.com)
- However, it is not a guarantee that glucose will completely counter the effects of cyanide, but it can reduce the effects. (healthontimeus.com)
Initially1
- She was initially fed carrots laced with potassium cyanide, then electrocuted and strangled. (yahoo.com)
Kills1
- Cyanide itself isn't dangerous, it's POTASSIUM cyanide that kills you. (todayifoundout.com)
Widely1
- Potassium Cyanide is widely used by entomologists as a killing agent in collecting jars, as most insects succumb within seconds, minimizing damage of even highly fragile specimens. (drjamesguerrero.com)
Urine1
- Excessive cystine in the urine may be detected with the nitroprusside cyanide test. (msdmanuals.com)
EXPOSURE1
- This public health statement tells you about cyanide and the effects of exposure to it. (cdc.gov)
Solution2
- How to analyze free cyanide in brass plating solution? (finishing.com)
- X-ray diffraction data were collected from native crystals and from identical crystals soaked in a solution containing potassium cyanide. (rcsb.org)
Spray1
- Indoor Air: Potassium cyanide can be released into indoor air as fine droplets, liquid spray (aerosol), or fine particles. (cdc.gov)
Naturally1
- Cyanides can both occur naturally or be man-made and many are powerful and rapid-acting poisons. (cdc.gov)
Successfully1
- Mr Denton duly received the potassium cyanide and successfully killed himself. (annaraccoon.com)
Deadly1
- Potassium may be the most well known, but it is certainly not the only deadly one. (todayifoundout.com)
Salt1
- Whole blood tube with lavender closure and EDTA potassium salt additive. (medscape.com)
Metals2
- Potassium helps in the extraction of gold and other precious metals in the mining industry. (healthontimeus.com)
- Cyanides form strong complexes with many metals, particularly those of the transition series. (cdc.gov)
Difficulties1
- I have difficulties analysing the free cyanide in brass. (finishing.com)
Search1
- police officers discovered the potassium cyanide under Ghane's kitchen sink while executing a search warrant at his apartment on Feb. 5, 2003. (justice.gov)