Paraquat
Herbicides
Maneb
Poisoning
Superoxide Dismutase
Oxidative Stress
Carbaryl
Perinatal nephropathies. (1/877)
The purpose of this paper is to review the development of the mammalian kidney and to assess the influence that various perinatal manipulations may have on the developmental process either morphologically or functionally. Immature kidneys in general have less functional capacity than adult kidneys and a low rate of glomerular filtration, perhaps related to renal blood flow, which appears to limit the disposition of a fluid or solute load. Tubular reabsorption is also limited leading to the urinary loss of glucose, amino acids, bicarbonate and phosphate. Although the relatively low function of the immature kidney is a normal part of development, its capacity to respond under conditions of stress may be less adequate than in adults. An additional concern is that a variety of perinatal manipulations, such as the incidental or accidental ingestion of a chemical, may lead to varying degrees of altered morphogenesis or functional development of the kidney. Chemical induced renal anomalies may be of several types, but in typical teratology experiments hydronephrosis may be the most frequent observation. The functional consequences of these renal malformations may be lethal or inconsequential or while an animal may be able to survive and develop normally in the presence of a renal malformation, it is possible that a stressful situation would unmask a functional malformation which could compromise survival. Thus, some renal abnormalities may be subtle enough to go unnoticed without experimental tests. Without such tests it is impossible to evaluate the effect of functional alterations on successful adaptation. (+info)SodA and manganese are essential for resistance to oxidative stress in growing and sporulating cells of Bacillus subtilis. (2/877)
We constructed a sodA-disrupted mutant of Bacillus subtilis 168, BK1, by homologous recombination. The mutant was not able to grow in minimal medium without Mn(II). The spore-forming ability of strain BK1 was significantly lower in Mn(II)-depleted medium than that of the wild-type strain. These deleterious effects caused by the sodA mutation were reversed when an excess of Mn(II) was used to supplement the medium. Moreover, the growth inhibition by superoxide generators in strain BK1 and its parent strain was also reversed by the supplementation with excess Mn(II). We therefore estimated the Mn-dependent superoxide-scavenging activity in BK1 cells. Whereas BK1 cells have no detectable superoxide dismutase (Sod) on native gel, the superoxide-scavenging activity in crude extracts of BK1 cells grown in Mn(II)-supplemented LB medium (10 g of tryptone, 5 g of yeast extract, and 5 g of NaCl per liter) was significantly detected by the modified Sod assay method without using EDTA. The results obtained suggest that Mn, as a free ion or a complex with some cellular component, can catalyze the elimination of superoxide and that both SodA and Mn(II) are involved not only in the superoxide resistance of vegetative cells but also in sporulation. (+info)Cytotoxic effect of paraquat on rat C6 glioma cells: evidence for the possibility of non-oxidative damage to the cells. (3/877)
Although paraquat has been shown to cause oxidative damage to neuronal cells, little is known about its effect on glial cells. Thus the effect of paraquat on glial cells was examined using rat C6 glioma cells as a model system. Paraquat reduced cell viability in a concentration- and time-dependent manner, and this toxic effect was not significantly attenuated by various kinds of antioxidants. Furthermore, paraquat failed to increase 8-hydroxy-deoxyguanosine formation in the cells. These results indicate that paraquat can be toxic to glial cells and suggest that this cytotoxic effect may not be associated with the oxidative damage to the cells. (+info)The alternative sigma factor, sigmaE, is critically important for the virulence of Salmonella typhimurium. (4/877)
In Escherichia coli, extracytoplasmic stress is partially controlled by the alternative sigma factor, RpoE (sigmaE). In response to environmental stress or alteration in the protein content of the cell envelope, sigmaE upregulates the expression of a number of genes, including htrA. It has been shown that htrA is required for intramacrophage survival and virulence in Salmonella typhimurium. To investigate whether sigmaE-regulated genes other than htrA are involved in salmonella virulence, we inactivated the rpoE gene of S. typhimurium SL1344 by allelic exchange and compared the phenotype of the mutant (GVB311) in vitro and in vivo with its parent and an isogenic htrA mutant (BRD915). Unlike E. coli, sigmaE is not required for the growth and survival of S. typhimurium at high temperatures. However, GVB311 did display a defect in its ability to utilize carbon sources other than glucose. GVB311 was more sensitive to hydrogen peroxide, superoxide, and antimicrobial peptides than SL1344 and BRD915. Although able to invade both macrophage and epithelial cell lines normally, the rpoE mutant was defective in its ability to survive and proliferate in both cell lines. The effect of the rpoE mutation on the intracellular behavior of S. typhimurium was greater than that of the htrA mutation. Both GVB311 and BRD915 were highly attenuated in mice. Neither strain was able to kill mice via the oral route, and the 50% lethal dose (LD50) for both strains via the intravenous (i.v.) route was very high. The i.v. LD50s for SL1344, BRD915, and GVB311 were <10, 5.5 x 10(5), and 1.24 x 10(7) CFU, respectively. Growth in murine tissues after oral and i.v. inoculation was impaired for both the htrA and rpoE mutant, with the latter mutant being more severely affected. Neither mutant was able to translocate successfully from the Peyer's patches to other organs after oral infection or to proliferate in the liver and spleen after i.v. inoculation. However, the htrA mutant efficiently colonized the livers and spleens of mice infected i.v., but the rpoE mutant did not. Previous studies have shown that salmonella htrA mutants are excellent live vaccines. In contrast, oral immunization of mice with GVB311 was unable to protect any of the mice from oral challenge with SL1344. Furthermore, i.v. immunization with a large dose ( approximately 10(6) CFU) of GVB311 protected less than half of the orally challenged mice. Thus, our results indicate that genes in the sigmaE regulon other than htrA play a critical role in the virulence and immunogenicity of S. typhimurium. (+info)Pre-steady-state kinetics of the reactions of [NiFe]-hydrogenase from Chromatium vinosum with H2 and CO. (5/877)
Results are presented of the first rapid-mixing/rapid-freezing studies with a [NiFe]-hydrogenase. The enzyme from Chromatium vinosum was used. In particular the reactions of active enzyme with H2 and CO were monitored. The conversion from fully reduced, active hydrogenase (Nia-SR state) to the Nia-C* state was completed in less than 8 ms, a rate consistent with the H2-evolution activity of the enzyme. The reaction of CO with fully reduced enzyme was followed from 8 to 200 ms. The Nia-SR state did not react with CO. It was discovered, contrary to expectations, that the Nia-C* state did not react with CO when reactions were performed in the dark. When H2 was replaced by CO, a Nia-C* EPR signal appeared within 11 ms; this was also the case when H2 was replaced by Ar. With CO, however, the Nia-C* state decayed within 40 ms, due to the generation of the Nia-S.CO state (the EPR-silent state of the enzyme with bound CO). The Nia-C* state, induced after 11 ms by replacing H2 by CO in the dark, could be converted, in the frozen enzyme, into the EPR-detectable state with CO bound to nickel (Nia*.CO) by illumination at 30 K (evoking the Nia-L* state), followed by dark adaptation at 200 K. This can be explained by assuming that the Nia-C* state represents a formally trivalent state of nickel, which is unable to bind CO, whereas nickel in the Nia-L* and the Nia*.CO states is formally monovalent. (+info)Nitroreductase A is regulated as a member of the soxRS regulon of Escherichia coli. (6/877)
Nitroreductase A catalyzes the divalent reduction of nitro compounds, quinones, and dyes by NADPH. In this paper, nitroreductase A is induced in Escherichia coli by exposure to paraquat in a manner that depends on the expression of soxR. Nitroreductase activity was only slightly induced by paraquat in a strain bearing a mutational defect in the gene encoding nitroreductase A, but it was approximately 3-fold induced in the parental strain. Nitroreductase A thus appears to be a member of the soxRS regulon and probably contributes to the defenses against oxidative stress by minimizing the redox cycling attendant upon the univalent reduction of nitro compounds, quinones, and dyes. (+info)Paraquat toxicity: proposed mechanism of action involving lipid peroxidation. (7/877)
The purpose of this study was to investigate the hypothesis that paraquat pulmonary toxicity results from cyclic reduction-oxidation of paraquat with sequential generation of superoxide radicals and singlet oxygen and initiation of lipid peroxidation. In vitro mouse lung microsomes catalyzed an NADPH-dependent, single-electron reduction of paraquat. Incubation of paraquat with NADPH, NADPH-cytochrome c reductase, and purified microsomal lipid increased malondialdehyde production is a concentration dependent manner. Addition of either superoxide dismutase or a single oxygen trapping agent 1,3-dipheylisobenzo furan inhibited paraquat stimulated lipid peroxidation. In vivo, pretreatment of mice with phenobarbital decreased paraquat toxicity, possibly by competing for electrons which might otherwise reduce paraquat. In contrast, paraquat toxicity in mice was increased by exposure to 100% oxygen and by deficiencies of the antioxidants selenium, vitamin E, or reduced glutahione (GSH). Paraquat, given IP to mice, at 30 mg/kg, decreased concentrations of the water-soluble antioxidant GSH in liver and lipid soluble antioxidants in lung. Oxygen-tolerant rats, which hae increased activities of pulmonary enzymes which combat lipid peroxidation, were also tolerant to lethal doses of paraquat as indicated by an increased paraquat LT50. Furthermore, rats chronically exposed to 100 ppm paraquat in the water had elevated pulmonary activities of glucose-6-phosphate dehydrogenase and GSH reductase. These results were consistent with the hypothesis that lipid peroxidation is involved in the toxicity of paraquat. (+info)Decreased intracellular superoxide levels activate Sindbis virus-induced apoptosis. (8/877)
Infection of many cultured cell types with Sindbis virus (SV), an alphavirus, triggers apoptosis through a commonly utilized caspase activation pathway. However, the upstream signals by which SV activates downstream apoptotic effectors, including caspases, remain unclear. Here we report that in AT-3 prostate carcinoma cells, SV infection decreases superoxide (O-2) levels within minutes of infection as monitored by an aconitase activity assay. This SV-induced decrease in O-2 levels appears to activate or modulate cell death, as a recombinant SV expressing the O-2 scavenging enzyme, copper/zinc superoxide dismutase (SOD), potentiates SV-induced apoptosis. A recombinant SV expressing a mutant form of SOD, which has reduced SOD activity, has no effect. The potentiation of SV-induced apoptosis by wild type SOD is because of its ability to scavenge intracellular O-2 rather than its ability to promote the generation of hydrogen peroxide. Pyruvate, a peroxide scavenger, does not affect the ability of wild type SOD to potentiate cell death; and increasing the intracellular catalase activity via a recombinant SV vector has no effect on SV-induced apoptosis. Moreover, increasing intracellular O-2 by treatment of 3T3 cells with paraquat protects them from SV-induced death. Altogether, our results suggest that SV may activate apoptosis by reducing intracellular superoxide levels and define a novel redox signaling pathway by which viruses can trigger cell death. (+info)Paraquat is a highly toxic herbicide that is used for controlling weeds and grasses in agricultural settings. It is a non-selective contact weed killer, meaning it kills any green plant it comes into contact with. Paraquat is a fast-acting chemical that causes rapid desiccation of plant tissues upon contact.
In a medical context, paraquat is classified as a toxicological emergency and can cause severe poisoning in humans if ingested, inhaled, or comes into contact with the skin or eyes. Paraquat poisoning can lead to multiple organ failure, including the lungs, kidneys, and liver, and can be fatal in severe cases. There is no specific antidote for paraquat poisoning, and treatment typically focuses on supportive care and managing symptoms.
It's important to note that paraquat is highly regulated and its use is restricted to licensed professionals due to its high toxicity. Proper protective equipment, including gloves, goggles, and respiratory protection, should be used when handling paraquat to minimize the risk of exposure.
Herbicides are a type of pesticide used to control or kill unwanted plants, also known as weeds. They work by interfering with the growth processes of the plant, such as inhibiting photosynthesis, disrupting cell division, or preventing the plant from producing certain essential proteins.
Herbicides can be classified based on their mode of action, chemical composition, and the timing of their application. Some herbicides are selective, meaning they target specific types of weeds while leaving crops unharmed, while others are non-selective and will kill any plant they come into contact with.
It's important to use herbicides responsibly and according to the manufacturer's instructions, as they can have negative impacts on the environment and human health if not used properly.
Maneb is not a term that has a widely accepted medical definition. However, in the field of agriculture and toxicology, Maneb is a commonly used fungicide to control various plant diseases. It is a complex organometallic compound containing manganese.
In some contexts, Maneb may be mentioned in relation to human health because it has been found to have potential reproductive and developmental effects, as well as being potentially carcinogenic. However, it is not considered a medical term or diagnosis. If you have any concerns about exposure to Maneb or its potential health effects, it would be best to consult with a healthcare professional.
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.
Medical Definition:
Superoxide dismutase (SOD) is an enzyme that catalyzes the dismutation of superoxide radicals (O2-) into oxygen (O2) and hydrogen peroxide (H2O2). This essential antioxidant defense mechanism helps protect the body's cells from damage caused by reactive oxygen species (ROS), which are produced during normal metabolic processes and can lead to oxidative stress when their levels become too high.
There are three main types of superoxide dismutase found in different cellular locations:
1. Copper-zinc superoxide dismutase (CuZnSOD or SOD1) - Present mainly in the cytoplasm of cells.
2. Manganese superoxide dismutase (MnSOD or SOD2) - Located within the mitochondrial matrix.
3. Extracellular superoxide dismutase (EcSOD or SOD3) - Found in the extracellular spaces, such as blood vessels and connective tissues.
Imbalances in SOD levels or activity have been linked to various pathological conditions, including neurodegenerative diseases, cancer, and aging-related disorders.
Oxidative stress is defined as an imbalance between the production of reactive oxygen species (free radicals) and the body's ability to detoxify them or repair the damage they cause. This imbalance can lead to cellular damage, oxidation of proteins, lipids, and DNA, disruption of cellular functions, and activation of inflammatory responses. Prolonged or excessive oxidative stress has been linked to various health conditions, including cancer, cardiovascular diseases, neurodegenerative disorders, and aging-related diseases.
Carbaryl is a carbamate pesticide that is used to control a wide variety of insects, including fleas, ticks, and mosquitoes. It works by inhibiting the action of an enzyme called cholinesterase, which is necessary for the proper functioning of the nervous system in insects. This leads to paralysis and death of the pests. Carbaryl is also used in some veterinary products to treat parasitic infestations. It can be found in various forms, such as powders, granules, and solutions, and can be applied to plants, animals, and indoor/outdoor surfaces. However, it can be harmful to non-target organisms, including humans, if not used properly. Therefore, it is important to follow the label instructions carefully when using carbaryl products.
Selenium oxides are inorganic compounds that contain selenium in an oxidized state combined with oxygen. The most common forms of selenium oxides include:
1. Selenium dioxide (SeO2): A red or yellow crystalline solid, selenium dioxide is formed by the oxidation of elemental selenium or by the burning of selenium in air. It is soluble in water and alcohol, forming selenous acid.
2. Selenium trioxide (SeO3): A white crystalline solid, selenium trioxide is a strong oxidizing agent that can react violently with reducing agents. It is used as a catalyst in the industrial production of certain chemicals and as a reagent in organic synthesis.
Selenium oxides have been studied for their potential use in various medical applications, such as antimicrobial agents and drug delivery systems. However, they are not currently used as therapeutic agents in clinical medicine due to their toxicity and potential health hazards.