Pesticide Biotransformation and Disposition
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Please review our Terms and Conditions of Use and check box below to share full-text version of article. Citing Literature. Volume 15 , Issue 5 October Pages Related Information. Close Figure Viewer. Browse All Figures Return to Figure. Previous Figure Next Figure. Email or Customer ID. Forgot password? Old Password. New Password. Catalases are known to facilitate the removal of hydrogen peroxide, which is metabolized by them to molecular oxygen and water.
Glutathione peroxidase GPx , which employs GSH as a cofactor, reduces many organic peroxides; its operation plays an especially important role in protecting the integrity of membranes under oxidative insults via prevention of lipid peroxidation Stegeman et al. Lipid peroxidation or oxidation of polyunsaturated fatty acids is a very important consequence of ROS attack to living organisms since it demonstrates the ability of a single radical species to propagate a number of deleterious biochemical reactions Stegeman et al.
It is known that some pesticides can cause oxidative stress by stimulating ROS generation Banerjee et al. Therefore, they are suspected to induce alterations in antioxidant and ROS-scavenging enzymatic systems. Pesticide-induced toxicity of many pollutants may be realized via stimulation of peroxidation of lipids Akhgari et al.
For example, long-term exposure to propiconazole was shown to cause ROS-promoted stress in several tissues of rainbow trout, O. Production of ROS can also be stimulated by phenoxy herbicides perhaps due to ROS formation by autoxidation, or a direct attack of the phenoxyl radicals on sensitive enzymes from a number of metabolic pathways Selassie et al.
Indeed, several studies demonstrated that 2,4-D induced oxidative stress and depleted antioxidants both in vitro and in vivo Bukowska, [ 20 ]; Kubrak et al. Herbicide paraquat can enter an autoxidation process resulting in the production of superoxide anion radicals Figure 9 Fig. As a free radical generator, paraquat has a redox potential of mV. Formed superoxide anion may be converted to hydrogen peroxide and hydroxyl radical Figure 9 Fig. Pulmonary effects as the result of ROS generation with extensive oxidative damage represent the most lethal and least treatable manifestation of paraquat toxicity in exposed animals Bolognesi and Merlo, [ 15 ].
Despite its structural similarity to paraquat, the mechanism of diquat toxicity was found to differ. It has been proposed that diquat stimulates ROS production by inhibition of complexes I and III of the mitochondrial electron transport chain Drechsel and Patel, [ 42 ]. In redox cycles, the parent compound is typically first reduced enzymatically by a NADPH-dependent reductase to yield a xenobiotic radical van der Oost et al. Thus, at each turn of the cycle, two potentially deleterious events occur: reductant oxidation and oxyradical formation Goeptar et al.
These processes induce either adaptive responses, such as increase in the activities of antioxidant enzymes and concentrations of low molecular mass antioxidants like glutathione, or manifestations of oxidant-mediated toxicity such as oxidations of proteins, lipids and nucleic acids, as well as perturbing tissue redox status Lushchak, [ ][ ], [ ]. A number of pesticides, such as vinclozolin, dicofol, atrazine, and others, belong to the class of chemicals called endocrine disruptors EDCs that are known to interfere with the production, release, transport, metabolism, action, or elimination of hormones responsible for maintenance of homeostasis and regulation of developmental processes Bolognesi and Merlo, [ 15 ]; Khan and Law, [ 91 ].
In fish, EDCs can cause male fish to transform into ones with female characteristics. These outward symptoms of developmental disruption are accompanied by reduced fertility or even sterility in adults, as well as lower hatching rates and viability of offsprings Ewing, [ 51 ]; Goodbred et al. Agonists may interact with hormone-binding proteins, and antagonists may displace endogenous hormones Tollefsen, [ ]. Some toxicants also disrupt the synthesis of hormone receptors Scott and Sloman, [ ].
The ultimate aim of reproduction is birth and its success depends upon both male and female reproductive systems Gupta, [ 68 ]. The decreased reproductive capability may be considered as one of the most damaging effects of the persistent pollutants e. The presence of these chemicals in the environment has become a global concern.
As blockers of sex hormone effects, pesticides may cause abnormal sexual development and other disturbances of other vital processes Ewing, [ 51 ]; Gupta, [ 68 ]. Although dioxin is not used as pesticide, in some cases it can arise as a contaminant at production of herbicides Manz et al. Dioxin is the most toxic and best-studied chemical that can lead to male reproductive toxicity Gupta, [ 68 ].
It causes functional developmental toxicity with additional structural abnormalities that are delayed in their appearance in multiple species. The effects of prenatal dioxin exposure on the reproductive system of female rats and hamsters indicated a delay in vaginal opening and clefting of the external genitalia Cooper et al. This may reflect a lack of appropriate differentiation. The herbicide atrazine has been proposed to exert adverse effects on the reproductive system of animals including mammals, fish, and amphibians Grasiela and Silva-Zacarin, [ 67 ].
Indeed, it is reported to disrupt ovarian function by altering hypothalamic control of the pituitary and the release of luteinizing hormone and prolactin in female rats Cooper et al. Ovarian cycle irregularities may be due to the ability of atrazine to interfere with hormone synthesis, binding to the estrogen receptor without activation Solomon et al. Similar effects were observed when atrazine degradation products were found to affect the onset of puberty and thyroid function in male rats via actions on the central nervous system and its subsequent control of the pituitary-gonadal axis Stoker et al.
There was also evidence of reproductive function impairment and depletion of the antioxidant defense system in rat testis and epididymis after exposure to atrazine Grasiela and Silva-Zacarin, [ 67 ]. It was observed that a single dose of benzimidazole carbamates induced rapid testicular effects, detectable as an increase in testis weight, but having long-term effects leading to testicular atrophy and infertility.
The inflammatory response with occluded ductules caused subsequent damage to the ductal epithelium. The rete testis was swollen with compacted sperm and the seminiferous tubules were atrophic with edematous interstitial space Nakai and Hess, [ ]. Dithiocarbamates are well-known endocrine disrupters that alter thyroid hormone levels and animal mass.
The number of healthy follicles was a significantly decreased, whereas thyroid gland weight was increased Baligar and Kaliwal, [ 5 ]. The hypothyroid and antithyroid effects of the fungicides zineb and mancozeb are associated with their metabolite ethinylthiourea Houeto et al. The action of ethinylthiourea on the thyroid gland with resultant hyperplasia and a decrease in thyroid hormone levels is the most prominent aspect of its toxicity Houeto et al.
Interestingly, ROS are not only associated with oxidative stress, but are also thought to play significant roles in reproduction Bongiovanni et al. Hence, induction of oxidative stress by pesticides has also been pointed out as a possible mechanism of some toxic effects on the reproductive system Abdollahi et al. Animal studies remain a valuable tool for detecting of potential human cancer hazards.
However, the evidence that a chemical causes tumors in experimental animals is considered sufficient only when experimental data show an increased incidence of malignant tumors in multiple species and following multiple routes Bolognesi and Merlo, [ 15 ]. A few pesticides e. The production of carcinogenic compounds such as N-nitrosocarbaryl, a derivative of carbaryl which is a potent carcinogen in rats is the principal hazard of these toxins Bolognesi and Merlo, [ 15 ].
Ethylene thiourea, a degradation product of ethylene bisdithiocarbamate fungicides, is also reported to be a teratogen, goitrogen, and carcinogen that can disrupt thyroid function and is causally related to thyroid cancer in animals Steenland et al. Thyroid-like effects of fungicides were observed in subchronic level studies of metiram-treated rats as evidenced by increased thyroid mass, increased levels of thyroid-stimulating hormone and decreased levels of T4 serum thyroxin U.
EPA, [ ]. The ethylene-bis-dithiocarbamates, in general, are considered to be carcinogenic because of their metabolite ETU Houeto et al. DA, [ ]. Calviello et al. Atrazine is one of the most important triazine herbicides used in large quantities worldwide. It has been identified as an endocrine disrupting chemical and a potential carcinogen Chelme-Ayala et al. The appearance of mammary tumors in atrazine-treated female rats has been documented Eldridge et al. Genotoxic compounds are those that act through direct or indirect DNA damage Bolognesi and Merlo, [ 15 ].
Many pesticides tested induced diverse mutations via DNA damage. The genotoxic potential of agrochemical ingredients is generally low, but occupational exposure to mixtures of pesticides has been associated with an increase in genotoxic damage in a number of studies Calviello et al. In laboratory tests, chlorothalonil fungicide caused kidney damage, anemia, liver damage, embryo loss during pregnancy, oxidative DNA damage, and cancers of the kidney and forestomach Oruc, [ ]. Most of these effects have been observed in several tested species.
Environmental Protection Agency Cox, [ 35 ]. Pesticide-induced oxidative stress is well-known to cause genotoxicity Franco et al. In general, pesticides have been shown to alter cellular redox balance enhancing ROS levels, lipid peroxidation, and depletion of antioxidant defenses Abdollahi et al.
Living organisms protect themselves from genotoxic and carcinogenic compounds in different ways. GSTs are an enzyme superfamily responsible for GSH conjugation with xenobiotics in their original or transformed forms and they might protect organisms against exogenous and endogenous toxicants Lushchak, [ ].
The activity of these enzymes in many cases can be altered by pesticide exposure Atamaniuk et al. It is known that the herbicide 2,3,7,8-tetrachlorodibenzodioxin is also an environmental teratogen. It affects cellular immunity in rodents and alters reproductive functions in the immature rat model through influences on the hypothalamic-pituitary axis as well by direct effects on the ovary Li et al. Teratology studies on 2,4-D indicated that malformations are likely to occur only at doses that are fetotoxic or maternally toxic USDA, [ ].
There is no doubt that pesticides influence the host's energy metabolism, nervous, cardiovascular, and endocrine systems, either directly or indirectly. It is clear that they cause many diseases, including metabolic syndrome, malnutrition, atherosclerosis, inflammation, pathogen invasion, nerve injury, and infectious disease susceptibility.
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Moreover, the listed pathologies may be aggravated in animals after exposure to pesticides. In this review, we discussed the classification of pesticides and their possible effects on non-target organisms. We further emphasized the importance and necessity of considering non-target living organisms as toxicological indicators for environmental pollution by pesticides. In the future, more studies should focus on the mechanisms of pesticide long-term influences on health. Moreover, the chronic duration of exposure to most contaminants may add another level of complexity that must also be considered in risk evaluation.
Future studies should be directed to minimize or eliminate influence of pesticides on non-target living organisms, produce more specific pesticides and using of modern technologies to decrease contamination of food and other goods by pesticides. We thank the many members of the V. Lushchak's laboratory who have contributed over the years: Drs. Bagnyukova, O. Kubrak, O. Lushchak, N. Semchuk Mosiichuk , H. Semchyshyn, O.
Vasylkiv, and I. Maksymiv, the research reviewed in this article. Figure 1: The movement of pesticide in the hydrologic cycle. Diffuse water pollution through pesticides occurs either due to evaporation 4 with short and long-distance transfer 5 , surface runoff 8 or leaching to groundwater Figure 2: Bioaccumulation of DDT in the food chain. Each successive consumer in the food chain accumulates contaminants to a higher level, thus magnifying the exposure when moving up the food chain. Figure 3: Biotransformation of pesticides. Description in the text. Figure 4: Cu-inhibitory sites and active sites of different electron donors and acceptors in PSII-mediated electron transport.
PSII, photosystem II; D1 and D2, bind the electron carriers involved in transfer of electrons from Tyr z to plastoquinone; b, cytochrome b; Tyr z , tyrosine residue active electron transfer from the manganese complex to reaction centre P; Pheo, pheophytin; Q A and Q B , bound plastoquinone; P, reaction center of chlorophyll primary electron donor ; PQ, reduced plastoquinone Husak, Description in the text Modified from Casida and Durkin Figure 6: Insecticide sites of action.
Some general methods of insecticide action are shown. Insecticides have many sites of action but most of those in common use affect the nervous system of the insect B. RT - renal tubules; H - hematopoietic tissue; N - necrotic cells and nuclei of tubular epithelium; MH - multiple hemorrhage; HT - hypertrophy of intertubular hematopoietic tissue; RC - red blood cells in necrotic tubules and Bowman's capsule; Fv - fatty vacuolization; Sy - sinusoids; Dh - detachment of endothelial cytoplasm with diffuse hemorrhage; Dhs - dystrophy of hepatic cells; Dec - detachment of endothelial cytoplasm modified from Husak et al.
Figure 8: Effect of organophosphorus insecticides in the transmission of nerve impulses: A - acetylcholine signaling at synapse; B - acetylcholinesterase stops signaling process; C - organophosphates inhibit acetylcholinesterase. Figure 9: Paraquat-induced oxidative stress. Modified from Dinis-Oliveira et al. Volodymyr I. Review article Pesticide toxicity: a mechanistic approach Volodymyr I.
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Diminishing returns: Salmon decline and pesticides. Funded by the Oregon pesticide education network, biotech research and consulting. Different responses of biochemical markers in frogs Rana ridibunda from urban and rural wetlands to the effect of carbamate fungicide. Catalysis of catechol oxidation by metal-dithiocarbamate complexes in pesticides. Free Radic Biol Med. Chem Biol Interact. Fukuto TR.
Biotransformation and disposition of hexachlorocyclopentadiene in fish
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A probabilistic aquatic ecological risk assessment of atrazine in North American surface waters. Dynamics of dietary bioaccumulation and fecal elimination of hydrophobic organic chemicals in fish. Oxygen reductase and substrate reductase activity of cytochrome P Effect of dithiocarbamate pesticide zineb and its commercial formulation, azzurro. Genotoxicity of the herbicide 2,4-dichlorophenoxyacetic and a commercial formulation, 2,4-dichlorophenoxyacetic acid dimethylamine salt.
Toxicol In Vitro. Reconnaissance of 17beta-estradiol, ketotestosterone, vitellogenin, and gonad histopathology in common carp of United States streams: Potential for contaminant-induced endocrine disruption. Sacramento, CA: U. S Geological Survey, Geological Survey Open-File Report Effects of herbicide atrazine in experimental animal models. Gupta PK.
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Herbicides and fungicides. In: Gupta RC ed : Reproductive and developmental toxicology pp Haddad JJ. Science review: redox and oxygen-sensitive transcription factors in the regulation of oxidant-mediated lung injury: role for hypoxia-inducible factor-1alpha. Crit Care. Chemical fate and transport in the environment. Hermes-Lima M. Oxidative stress and medical sciences. In: Storey KB ed : Functional metabolism: regulation and adaptation pp New York: Wiley, Liver structural alterations accompanying chronic toxicity: potential biomarkers of exposure.
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Husak V. Copper and copper-containing pesticides: metabolism, toxicity and oxidative stress. Histopathological and biochemical changes in goldfish kidney due to exposure to the herbicide Sencor may be related to induction of oxidative stress. Acute exposure to the penconazole-containing fungicide Topas partially augments antioxidant potential in goldfish tissues.
Hematological parameters in Nile Tilapia, Oreochromis niloticus exposed to sub-lethal concentrations of mercury. Braz Arch Biol Technol. Jablonkai I. Molecular mechanism of function of herbicides. James MO. Pesticide metabolism in aquatic organisms. Chem Plant Prot. Organochlorine pesticides, their toxic effects on living organisms and their fate in the environment. Interdiscip Toxicol.
Chlorpyrifos: pollution and remediation. Environ Chem Lett. Kamijima1 M, Casida JE. Regional modification of [3H]ethynylbicycloorthobenzoate binding in mouse brain GABAA receptor by endosulfan, fipronil, and avermectin B1a. Katagi T. Bioconcentration, bioaccumulation, and metabolism of pesticides in aquatic organisms.
Uptake, elimination and biotransformation of the lampricide 3-trifluoromethylnitrophenol TFM by larvae of the aquatic midge Chironomus tentans. Kennedy CJ. New York: Elsevier Science, Adverse effects of pesticides and related chemicals on enzyme and hormone systems of fish, amphibians and reptiles: A review. Proc Pakistan Acad Sci. Format: Kindle Edition. It's a dry book, as you'd expect, but as a non-expert I learned a lot about the complexity of pesticide metabolism. More importantly, it provides a great starting point for more in-depth research about a particular pesticide as the references for each chapter are extensive.
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