Fumigation
Insecticides
Trichlorfon
Cholinesterase Inhibitors
Acetylcholinesterase
Dimethoate
Blattellidae
Aflatoxins
Poisoning
Pesticides
Africa, Western
Pitfalls when determining tissue distributions of organophosphorus chemicals: sodium fluoride accelerates chemical degradation. (1/71)
This paper describes the tissue distributions of dichlorvos, an organophosphate, and chlorpyrifos-methyl, an organophosphorothioate, in a male individual who died after ingesting an insecticidal preparation containing these chemicals and the results of an in vitro stability study on dichlorvos and chlorpyrifos-methyl in blood and buffers. Tiny amounts of dichlorvos, 0.067 and 0.027 mg/L, were detected in the vitreous humor and cerebrospinal fluid, respectively. Although dichlorvos (0.082-8.99 mg/L or mg/kg) was detected in the thoracic aortic blood, thoracic inferior vena caval blood, pericardial fluid, bile, and spleen, it was strongly suggested that it had diffused postmortem from the stomach, which contained 879 mg, because no dichlorvos was detected in the other blood samples and tissues tested. Substantial amounts (0.615-4.15 mg/L) of chlorpyrifos-methyl were detected in all blood samples, and the order of its concentrations was as follows: pulmonary vessel blood > thoracic inferior vena caval blood > blood in the right cardiac chambers > blood in the left cardiac chambers approximately thoracic aortic blood > right femoral venous blood. The total amount of chlorpyrifos-methyl in the stomach was 612 mg. However, it was strongly suggested that virtually no chlorpyrifos-methyl diffused from the stomach into surrounding fluids and tissues postmortem because no chlorpyrifos-methyl was detected in the bile and little was found in the pericardial fluids. Neither compound was detected in the urine. In vitro experiments showed that dichlorvos (10 mg/L) almost disappeared from fresh (pH 7.4) and acidified (pH 6.2) blood samples within 24 and 72 h, respectively. However, 53 and 77% of the original amount of dichlorvos in 0.05M phosphate buffers at pH 7.4 and 6.2 were detected 72 h later. Chlorpyrifos-methyl (1 mg/L) was very stable in blood samples, regardless of the pH, during the 72-h study period, but in the pH 7.4 and 6.2 phosphate buffers, approximately 80% of the original amount had degraded after 72 h. These results indicate that organophosphates are degraded more rapidly by esterase activities than by chemical mechanisms and that organophosphorothioates are hydrolyzed chemically in aqueous solutions but are very stable in biological specimens and not metabolized by esterases. When sodium fluoride was added to blood samples, dichlorvos degraded completely within 15 min, and chlorpyrifos-methyl became very unstable. Thus, when analyzing samples to detect organophosphorus chemicals, this common preservative should not be added to fluid specimens. (+info)Identification of acylpeptide hydrolase as a sensitive site for reaction with organophosphorus compounds and a potential target for cognitive enhancing drugs. (2/71)
We describe here the purification and identification of a previously unrecognized target for organophosphorus compounds. The target, acylpeptide hydrolase, was isolated as a tritiated-diisopropylfluorophosphate-reactive protein from porcine brain and purified to homogeneity using a combination of ion-exchange and gel-filtration chromatography. Biochemical characterization and internal sequence analysis confirmed identity. Acylpeptide hydrolase was found to be potently inhibited by the organophosphorus compounds chlorpyrifosmethyl oxon, dichlorvos, and diisopropylfluorophosphate (20-min IC(50) values of 18.3 +/- 2.0, 118.7 +/- 9.7, and 22.5 +/- 1.2 nM, respectively). The in vitro sensitivity of acylpeptide hydrolase toward these compounds is between six and ten times greater than that of acetylcholinesterase (AChE), making it a target of pharmacological and toxicological significance. We show that, in vivo, acylpeptide hydrolase is significantly more sensitive than AChE to inhibition by dichlorvos and that the inhibition is more prolonged after a single dose of inhibitor. Furthermore, using dichlorvos as a progressive inhibitor, it was possible to show that acylpeptide hydrolase is the only enzyme in the brain capable of hydrolyzing the substrate N-acetyl-alanyl-p-nitroanilide. A concentration of 154 +/- 27 pmol of acylpeptide hydrolase/gram of fresh rat brain was also deduced by specific labeling with tritiated-diisopropylfluorophosphate. We also suggest that, by comparison of structure-activity relationships, acylpeptide hydrolase may be the target for the cognitive-enhancing effects of certain organophosphorus compounds. Acylpeptide hydrolase cleaves N(alpha)-acylated amino acids from small peptides and may be involved in regulation of neuropeptide turnover, which provides a new and plausible mechanism for its proposed cognitive enhancement effect. (+info)Retention of cytoplasmic droplet by rat cauda epididymal spermatozoa after treatment with cytotoxic and xenobiotic agents. (3/71)
Spermatozoa leaving the testis contain a cytoplasmic droplet which they release during transit through the epididymis before reaching the cauda epididymidis. The cytoplasmic droplet shows P450 aromatase activity, which plays a role in synthesis of oestrogen from androgen. In the present study, 3-month-old Wistar strain male albino rats were administered with the organophosphate insecticides malathion or dichlorvos, or the phytotherapeutics andrographolide or ursolic acid. Segments of the epididymis were subjected to histopathological and ultrastructural analyses and it was found that 60-95% of the spermatozoa residing in the lumen of the cauda epididymidis retained the cytoplasmic droplet. The motility of the spermatozoa released from the cauda epididymidis was inhibited. One of the mechanisms of action of these toxicants on male reproductive function may be attributed to the retention of the cytoplasmic droplet and the resultant impairment of sperm motility. (+info)Effects of S-ethyl hexahydro-1H-azepine-1-carbothioate (molinate) on di-n-butyl dichlorovinyl phosphate (DBDCVP) neuropathy. (4/71)
Certain esterase inhibitors protect from organophosphate-induced delayed polyneuropathy (OPIDP) when given before a neuropathic organophosphate by inhibiting neuropathy target esterase (NTE). In contrast, they can exaggerate OPIDP when given afterwards and this effect (promotion) is associated with inhibition of another esterase (M200). In vitro sensitivities of hen, rat, and human NTE and M200 to the active metabolites of molinate, sulfone, and sulfoxide, were similar. NTE and M200 were irreversibly inhibited (> 78%) in brain and peripheral nerve of hens and rats given molinate (100-180 mg/kg, sc). No clinical or morphological signs of neuropathy developed in these animals. Hens and rats were protected from di-n-butyl dichlorovinyl phosphate neuropathy (DBDCVP, 1 and 5 mg/kg, sc, respectively) by molinate (180 or 100 mg/kg, sc, 24 h earlier, respectively) whereas 45 mg/kg, sc molinate causing about 34% NTE inhibition offered partial protection to hens. Hens treated with DBDCVP (0.4 mg/kg, sc) developed a mild OPIDP; molinate (180 mg/kg, 24 h later) increased the severity of clinical effects and of histopathology in spinal cord and in peripheral nerves. Lower doses of molinate (45 mg/kg, sc), causing about 47% M200 inhibition, did not promote OPIDP whereas the effect of 90 mg/kg, sc (corresponding to about 50-60% inhibition) was mild and not statistically significant. OPIDP induced by DBDCVP (5 mg/kg, sc) in rats was promoted by molinate (100 mg/kg, sc). In conclusion, protection from DBDCVP neuropathy by molinate is correlated with inhibition of NTE whereas promotion of DBDCVP neuropathy is associated with > 50% M200 inhibition. (+info)Short- and long-term effect of acetylcholinesterase inhibition on the expression and metabolism of the amyloid precursor protein. (5/71)
We have investigated the acute and chronic effect of metrifonate (MTF) and dichlorvos (DDVP), respectively the prodrug and active acetylcholinesterase inhibitor, on the secretory processing of the amyloid precursor protein (APP) in SH-SY5Y neuroblastoma cells. We demonstrate that the acute treatment of SH-SY5Y cells with both compounds results in an increased secretion of the soluble fragment of APP (sAPPalpha) into the conditioned media of cells, with a pattern correlated to the level of acetycholinesterase inhibition. The regulation of APP processing in these conditions is mediated by an indirect cholinergic effect on muscarinic receptors, as demonstrated by inhibition with atropine. We have also followed APP expression and metabolism after long-term treatment with metrifonate. Treated cells showed reduced AChE activity after 24, 48 h and also following 7 days of repeated treatment, a time point at which increased AChE expression was detectable. At all time points sAPPalpha release was unaffected suggesting that enhanced sAPPalpha release by MTF is transitory, nevertheless the sensitivity of cholinergic receptors was unchanged, as indicated by the fact that cholinergic response can be elicited similarly in untreated and treated cells. APP gene expression was unaffected by long-term AChE inhibition suggesting that increased short-term sAPPalpha release does not elicit compensatory effects. (+info)Proposal for a method for testing resistance of clothing and gloves to penetration by pesticides. (6/71)
The paper presents the proposal for a method for testing the resistance of materials used for the production of protective clothing and gloves to penetration by concentrated chemical preparations of pesticides. It has been based to a large extent on the recommendations of European standards, with certain modifications resulting from the specific properties of non-volatile and non-water-soluble biologically-active components of pesticides. These modifications primarily involved the use of a solid sorption medium and adjustment of research apparatus to the research conditions consistent with the proposed method. The results of preliminary studies on penetration of the selected biologically-active components of pesticides (dichlorvos, 2,4-D, cypermethrin, carbofuran) through the selected protective materials (fabric coated with viton and butyl on both sides, rubberised fabric, butyl rubber) are presented. The study confirmed the usefulness of the proposed method for testing the resistance of materials protecting against the effect of pesticides. (+info)Acetylcholinesterase engineering for detection of insecticide residues. (7/71)
To detect traces of insecticides in the environment using biosensors, we engineered Drosophila acetylcholinesterase (AChE) to increase its sensitivity and its rate of phosphorylation or carbamoylation by organophosphates or carbamates. The mutants made by site-directed mutagenesis were expressed in baculovirus. Different strategies were used to obtain these mutants: (i) substitution of amino acids at positions found mutated in AChE from insects resistant to insecticide, (ii) mutations of amino acids at positions suggested by 3-D structural analysis of the active site, (iii) Ala-scan analysis of amino acids lining the active site gorge, (iv) mutagenesis at positions detected as important for sensitivity in the Ala-scan analysis and (v) combination of mutations which independently enhance sensitivity. The results highlighted the difficulty of predicting the effect of mutations; this may be due to the structure of the site, a deep gorge with the active serine at the bottom and to allosteric effects between the top and the bottom of the gorge. Nevertheless, the use of these different strategies allowed us to obtain sensitive enzymes. The greatest improvement was for the sensitivity to dichlorvos for which a mutant was 300-fold more sensitive than the Drosophila wild-type enzyme and 288 000-fold more sensitive than the electric eel enzyme, the enzyme commonly used to detect organophosphate and carbamate. (+info)Organophosphate-induced delayed neuropathy: case report. (8/71)
Organophosphate induced delayed neuropathy (OPIDN) is an uncommon clinical condition. It occurs in association with the ingestion of great amounts of organophosphate after the stimulation of cholinergic receptor. The clinical picture is characterized by a distal paresis in lower limbs associated with sensitive symptoms. Electrodiagnostic studies show a motor axonal neuropathy. Involvement of the central nervous system may occur. We describe a 39 years-old female patient who developed hyperesthesia associated with lower limbs paresis, fourteen days after she had ingested a Dichlorvos-based insecticide. Electrophysiological study was characterized by an axonal polyneuropathy pattern. Pyramidal tract dysfunction was observed later in upper limbs. Considering that both peripheral and central nervous systems are involved we believe that the more appropriated term would be organophosphate induced delayed neuropathy (OPIDN) instead of organophosphate induced delayed polyneuropathy (OPIDP). (+info)Dichlorvos is a type of organophosphate insecticide that is used to control a wide variety of pests in agricultural, residential, and industrial settings. Its chemical formula is (2,2-dichlorovinyl) dimethyl phosphate. It works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine in the synaptic clefts of nerve cells, causing overstimulation of the nervous system and ultimately death of the pest.
Dichlorvos is highly toxic to both insects and mammals, including humans. Exposure to this chemical can cause a range of symptoms, including headache, dizziness, nausea, vomiting, muscle weakness, and in severe cases, respiratory failure and death. It is classified as a Category I acute toxicant by the Environmental Protection Agency (EPA) and is listed as a hazardous substance under the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA).
Due to its high toxicity and potential for environmental persistence, dichlorvos is subject to strict regulations in many countries. It is banned or restricted for use in several jurisdictions, including the European Union, Canada, and some states in the United States. Where it is still allowed, it is typically used only under specific conditions and with appropriate safety measures in place.
Fumigation is not typically considered a medical term, but it does have relevance to public health and environmental medicine. According to the World Health Organization (WHO), fumigation is defined as "the treatment of a building or commodity by introducing a gaseous pesticide (fumigant) in sufficient concentration to kill all stages of pests present."
Fumigation is used to control pests, such as insects, rodents, and other organisms that can cause harm to human health, property, or the environment. It is commonly used in agriculture to protect stored commodities from pests during transportation and storage. In addition, fumigation may be used in public health to disinfect buildings, equipment, and other items that have been infested with pests, such as bed bugs, cockroaches, or termites.
Fumigants are toxic gases that can cause harm to humans and animals if not handled properly. Therefore, fumigation should only be carried out by trained professionals who follow strict safety protocols to protect people, pets, and the environment from exposure.
Insecticides are substances or mixtures of substances intended for preventing, destroying, or mitigating any pest, including insects, arachnids, or other related pests. They can be chemical or biological agents that disrupt the growth, development, or behavior of these organisms, leading to their death or incapacitation. Insecticides are widely used in agriculture, public health, and residential settings for pest control. However, they must be used with caution due to potential risks to non-target organisms and the environment.
Trichlorfon is an organophosphate insecticide and acaricide. It is used to control a wide variety of pests, including flies, ticks, and mites in agriculture, livestock production, and public health. Trichlorfon works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine and results in paralysis and death of the pest. It is important to note that trichlorfon can also have harmful effects on non-target organisms, including humans, and its use is regulated by various governmental agencies to minimize potential risks.
Propoxur is a carbamate insecticide that acts as a cholinesterase inhibitor. It is used to control a wide variety of pests, including cockroaches, ants, fleas, and ticks. Propoxur works by disrupting the nervous system of insects, leading to paralysis and death. It can be found in various forms such as powders, granules, and liquids for use in residential and commercial settings. However, it is important to note that propoxur can also have toxic effects on non-target organisms, including humans, and its use is regulated by environmental and health agencies worldwide.
Cholinesterase inhibitors are a class of drugs that work by blocking the action of cholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine in the body. By inhibiting this enzyme, the levels of acetylcholine in the brain increase, which can help to improve symptoms of cognitive decline and memory loss associated with conditions such as Alzheimer's disease and other forms of dementia.
Cholinesterase inhibitors are also used to treat other medical conditions, including myasthenia gravis, a neuromuscular disorder that causes muscle weakness, and glaucoma, a condition that affects the optic nerve and can lead to vision loss. Some examples of cholinesterase inhibitors include donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon).
It's important to note that while cholinesterase inhibitors can help to improve symptoms in some people with dementia, they do not cure the underlying condition or stop its progression. Side effects of these drugs may include nausea, vomiting, diarrhea, and increased salivation. In rare cases, they may also cause seizures, fainting, or cardiac arrhythmias.
Diazinon is a type of organophosphate insecticide that works by inhibiting the enzyme acetylcholinesterase, which leads to an accumulation of the neurotransmitter acetylcholine in the synaptic cleft and results in overstimulation of cholinergic receptors. This can cause a variety of symptoms, including muscle twitching, tremors, convulsions, and respiratory failure, which can be fatal if not treated promptly.
Diazinon is used to control a wide range of insect pests in agriculture, horticulture, and residential settings. However, it is highly toxic to both insects and mammals, including humans, and its use is regulated by environmental and public health agencies around the world. Exposure to diazinon can occur through inhalation, skin contact, or ingestion, and can cause acute and chronic health effects depending on the level and duration of exposure.
In the medical field, diazinon poisoning is treated with atropine, which blocks the action of acetylcholine at muscarinic receptors, and oximes, which reactivate acetylcholinesterase. Supportive care, such as oxygen therapy, mechanical ventilation, and fluid replacement, may also be necessary in severe cases.
Acetylcholinesterase (AChE) is an enzyme that catalyzes the hydrolysis of acetylcholine (ACh), a neurotransmitter, into choline and acetic acid. This enzyme plays a crucial role in regulating the transmission of nerve impulses across the synapse, the junction between two neurons or between a neuron and a muscle fiber.
Acetylcholinesterase is located in the synaptic cleft, the narrow gap between the presynaptic and postsynaptic membranes. When ACh is released from the presynaptic membrane and binds to receptors on the postsynaptic membrane, it triggers a response in the target cell. Acetylcholinesterase rapidly breaks down ACh, terminating its action and allowing for rapid cycling of neurotransmission.
Inhibition of acetylcholinesterase leads to an accumulation of ACh in the synaptic cleft, prolonging its effects on the postsynaptic membrane. This can result in excessive stimulation of cholinergic receptors and overactivation of the cholinergic system, which may cause a range of symptoms, including muscle weakness, fasciculations, sweating, salivation, lacrimation, urination, defecation, bradycardia, and bronchoconstriction.
Acetylcholinesterase inhibitors are used in the treatment of various medical conditions, such as Alzheimer's disease, myasthenia gravis, and glaucoma. However, they can also be used as chemical weapons, such as nerve agents, due to their ability to disrupt the nervous system and cause severe toxicity.
Dimethoate is an organophosphate insecticide and acaricide (a chemical that kills mites). Its chemical formula is C5H12NO3PS. It works by inhibiting the activity of an enzyme called acetylcholinesterase, which is necessary for the proper functioning of the nervous system in both insects and mammals, including humans. This leads to an overstimulation of the nervous system, causing a variety of symptoms such as muscle twitching, tremors, convulsions, and eventually respiratory failure and death in severe cases.
Dimethoate is used to control a wide range of pests, including aphids, thrips, leafminers, and spider mites, on various crops such as fruits, vegetables, cereals, and ornamental plants. However, due to its toxicity to non-target organisms, including humans, it is important to use it with caution and follow all safety guidelines when handling and applying this chemical. It is also subject to regulations regarding its use and disposal in many countries.
Blattellidae is a family of small to medium-sized insects commonly known as cockroaches or wood cockroaches. They are closely related to the larger Blaberidae family, which includes many of the tropical cockroaches. Blattellidae species are found worldwide and include some of the most common and widespread cockroaches, such as the German cockroach (Blattella germanica) and the brown-banded cockroach (Supella longipalpa).
These insects are generally small, with adults ranging in size from about 1/2 to 3/4 inch (1.2 to 1.9 centimeters) in length. They have a flattened body and long, slender antennae. The wings of Blattellidae species are well-developed, but they are not strong flyers. Instead, they tend to scuttle quickly away when disturbed.
Blattellidae cockroaches are omnivorous, feeding on a wide variety of plant and animal materials. They can be found in a range of habitats, including forests, grasslands, and urban environments. Some species are adapted to living in close association with humans and can be found in homes, restaurants, and other buildings.
Like all cockroaches, Blattellidae species have the potential to carry and transmit diseases, as well as cause allergic reactions in some people. It is important to take steps to prevent and control infestations of these pests in order to maintain a healthy living environment.
Aflatoxins are toxic compounds produced by certain types of mold (Aspergillus flavus and Aspergillus parasiticus) that grow on crops such as grains, nuts, and spices. These toxins can contaminate food and animal feed, posing a serious health risk to both humans and animals. Aflatoxin exposure has been linked to various health problems, including liver damage, cancer, immune system suppression, and growth impairment in children. Regular monitoring and control measures are necessary to prevent aflatoxin contamination in food and feed supplies.
Poisoning is defined medically as the harmful, sometimes fatal, effect produced by a substance when it is introduced into or absorbed by living tissue. This can occur through various routes such as ingestion, inhalation, injection, or absorption through the skin. The severity of poisoning depends on the type and amount of toxin involved, the route of exposure, and the individual's age, health status, and susceptibility. Symptoms can range from mild irritation to serious conditions affecting multiple organs, and may include nausea, vomiting, diarrhea, abdominal pain, difficulty breathing, seizures, or unconsciousness. Immediate medical attention is required in cases of poisoning to prevent severe health consequences or death.
Butyrylcholinesterase (BChE) is an enzyme that catalyzes the hydrolysis of esters of choline, including butyrylcholine and acetylcholine. It is found in various tissues throughout the body, including the liver, brain, and plasma. BChE plays a role in the metabolism of certain drugs and neurotransmitters, and its activity can be inhibited by certain chemicals, such as organophosphate pesticides and nerve agents. Elevated levels of BChE have been found in some neurological disorders, while decreased levels have been associated with genetic deficiencies and liver disease.
Pesticides are substances or mixtures of substances intended for preventing, destroying, or repelling pests. Pests can be insects, rodents, fungi, weeds, or other organisms that can cause damage to crops, animals, or humans and their living conditions. The term "pesticide" includes all of the following: insecticides, herbicides, fungicides, rodenticides, bactericides, and various other substances used to control pests.
It is important to note that while pesticides are designed to be toxic to the target pests, they can also pose risks to non-target organisms, including humans, if not used properly. Therefore, it is essential to follow all label instructions and safety precautions when handling and applying pesticides.
"Western Africa" is a geographical region that consists of several countries located in the western part of the African continent. The United Nations defines Western Africa as the 16 countries of Benin, Burkina Faso, Cape Verde, Gambia, Ghana, Guinea, Guinea-Bissau, Ivory Coast, Liberia, Mali, Mauritania, Niger, Nigeria, Senegal, Sierra Leone, and Togo.
The region is characterized by a diverse range of cultures, languages, and ethnic groups, as well as a variety of landscapes, including coastal areas, savannas, and deserts. Western Africa has a rich history, with many ancient kingdoms and empires having existed in the region, such as the Ghana Empire, Mali Empire, and Songhai Empire.
In medical contexts, "Western Africa" may be used to describe the epidemiology, distribution, or characteristics of various health conditions or diseases that are prevalent in this geographical region. For example, certain infectious diseases such as malaria, HIV/AIDS, and Ebola virus disease are more common in Western Africa than in other parts of the world. Therefore, medical researchers and practitioners may use the term "Western Africa" to refer to the specific health challenges and needs of the populations living in this region.
Organophosphate (OP) poisoning refers to the toxic effects that occur after exposure to organophosphate compounds, which are commonly used as pesticides, nerve agents, and plasticizers. These substances work by irreversibly inhibiting acetylcholinesterase, an enzyme that breaks down the neurotransmitter acetylcholine in the nervous system. As a result, excessive accumulation of acetylcholine leads to overstimulation of cholinergic receptors, causing a wide range of symptoms.
The severity and type of symptoms depend on the dose, duration, and route of exposure (inhalation, ingestion, or skin absorption). The primary manifestations of organophosphate poisoning are:
1. Muscarinic effects: Excess acetylcholine at muscarinic receptors in the parasympathetic nervous system results in symptoms such as narrowed pupils (miosis), increased salivation, lacrimation, sweating, bronchorrhea (excessive respiratory secretions), diarrhea, bradycardia (decreased heart rate), and hypotension.
2. Nicotinic effects: Overstimulation of nicotinic receptors at the neuromuscular junction leads to muscle fasciculations, weakness, and paralysis. This can also cause tachycardia (increased heart rate) and hypertension.
3. Central nervous system effects: OP poisoning may result in headache, dizziness, confusion, seizures, coma, and respiratory depression.
Treatment for organophosphate poisoning includes decontamination, supportive care, and administration of antidotes such as atropine (to block muscarinic effects) and pralidoxime (to reactivate acetylcholinesterase). Delayed treatment can lead to long-term neurological damage or even death.