Effects on antioxidant status of liver following atrazine exposure and its attenuation by vitamin E
Introduction
Herbicides control or kill plants through a variety of mechanisms, including the inhibition of biological processes, such as photosynthesis, mitosis, cell division, enzyme function, root growth, or leaf formation, interference with the synthesis of pigments, protein or DNA, destruction of cell membranes; or the promotion of uncontrolled growth (William et al., 1995). Atrazine is a triazine herbicide that is used as a selective pre-emergence and post-emergence herbicide for the control of weeds in asparagus, maize, sorghum, sugarcane and pineapple. It is also used in forestry and for non-selective weed control on non-crop areas. It has been employed extensively in agriculture in the US and worldwide for over 40 years (Worthing 1991; US EPA, 1994). Atrazine is readily absorbed through the gastrointestinal tract. On administration of a single dose of atrazine (0.53 mg) to rats by gavage, 20% of it was excreted in feces within 72 h and 80% was absorbed across the gastrointestinal tract into the bloodstream (Hayes and Laws, 1990). Human exposure pathways for this chemical include occupational exposure through both inhalation and dermal absorption during its manufacture, its formulation and its application by spraying. Although, atrazine generally has low level of bioaccumulation in fish, it does accumulate in brain, gall bladder, liver and gut of some fishes (Eisler, 1989). Therefore, consumption of contaminated fish can also contribute to human exposure. Earlier studies from our laboratory have suggested that atrazine induces genotoxicity in liver and alters erythrocyte membrane structure in rats (Singh et al., 2008a, Singh et al., 2008b).
Previously, Gojmerac et al. (1995) had reported hepatic degeneration in pigs following atrazine exposure. Pesticides and herbicides induce hepatotoxicity, as liver is major site for detoxification of these compounds. The detoxification reactions of atrazine can be divided into phase I and phase II reactions. The major phase I metabolic reaction in plants and mammals is cytochrome P450-mediated N-dealkylation, while the phase II reaction is the glutathione-s-transferases (GST) catalyzed conjugation with glutathione (GSH) (Elia et al., 2002). Herbicides such as paraquat are known to exert their effects by inducing oxidative stress in tissues of mammals and fish (Winston and Di Giulio,1991). To prevent oxidation-induced damage, there are effective antioxidant systems in organisms. Some components of these systems are GSH and certain antioxidant enzymes including free radical scavenging enzymes, such as glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase. Other associated antioxidant enzymes are glutathione reductase (GR) and GST.
Non-enzymatic antioxidants such as α-tocopherol (vitamin E), ascorbate (vitamin C), β-carotene (vitamin A), flavonoids (quercetin, rutin, etc.), selenium and thiol containing compounds such as glutathione (GSH) can also act to overcome the oxidative stress, being a part of total antioxidant system (Sies et al., 1992). Vitamin E is an important biological free radical scavenger in the cell membranes (Horwitt, 1976). In the present investigation we studied whether vitamin E has the potential to attenuate atrazine-induced oxidative stress.
Section snippets
Chemicals
Atrazine (technical grade 97.83%) was a gift from Meghmani Industries Ltd. (India). Vitamin E (α-tocopheryl acetate, trade name – Evion) was obtained from Merck Pharmaceuticals, India. All other chemicals used were of analytical grade procured from local commercial sources.
Animals
Male rats (wistar strain), weighing about 100–120 g, were used throughout the studies. The animals were procured from the Central Animal House of the Panjab University. The animals were housed in polypropylene cages, provided
Body weight and liver weight
The changes in the body weight of the animals of various groups are shown in Table 1. A progressive increase in the body weight of rats was observed in the control and vitamin E treated groups. Maximum gain in the body weight was observed in the vitamin E treated rats as compared to all other groups. The administration of atrazine resulted in the loss of body weight of the rats. The reduction in body weight was pronounced in animals treated with atrazine for 21 days. After exposure with
Discussion
The decrease in the body weight following atrazine administration is in accordance with reports in literature of decrease in body weight following exposure to pesticides (Kennedy, 1986; Sharma et al., 2005). Roloff et al. (1992) observed decrease in body weight after the atrazine administration in mice. The decrease in the body weight after atrazine administration could be due to reduced diet intake or due to necrotic changes in the various body tissues (Gojmerac et al.,1995). The gain in body
Conclusion
From the above observations it can be concluded that exposure of atrazine results in increased oxidative stress and altered antioxidant status of the liver. Administration of vitamin E along with atrazine resulted in partial normalization of the toxic effects of atrazine thus highlighting the protective action of vitamin E.
References (62)
- et al.
Protective effects of antioxidants against endrin-induced hepatic lipid peroxidation, DNA damage and excretion of urinary lipid metabolites
Free Radical Biol Med
(1993) - et al.
A comparative study of effects of atrazine on xenobiotics metabolizing enzymes in fish and insects, and of the in vitro phase-II atrazine metabolism in some fish, insects, mammals, and one plant species
Comp Biochem Physiol C
(1993) - et al.
A new and rapid colorimetric determination of acetylcholinesterase activity
Biochem Pharmacol
(1961) - et al.
Glutathione-S-transferase. The first enzymatic step in mercapturic acid formation
J Biol Chem
(1974) - et al.
In vitro metabolism of chlorotiazines: characterization of simazine, atrazine, and propazine metabolism using liver microsomes from rats with various cytochrome P450 inducers
Toxicol Appl Pharmacol
(1999) Vitamin E: a reexamination
Am J Clin Nutr
(1976)- et al.
Protective effect of vitamin E in dimethoate and malathion induced oxidative stress in rat erythrocytes
J Nutr Biochem
(2001) Chronic toxicity, reproductive, and teratogenic studies with oxamly
Fundam Appl Toxicol
(1986)Generation of superoxide radical during autoxidation of hydroxylamine and an assay for superoxide dismutase
Arch Biochem Biophys
(1978)- et al.
Glutathione peroxidase activity in selenium-deficient rat liver
Biochem Biophys Res Commun
(1976)
Dietary supplements of vitamin E, beta-carotene, coenzyme Q10 and selenium protect tissues against lipid peroxidation in rat tissue slices
J Nutr
Protein measurement with the folin phenol reagent
J Biol Chem
Superoxide dismutase: an enzymatic function for erythrocuprein (hemocuprein)
J Biol Chem
Vitamin E protection against chemical induced cell injury. I. Maintenance of cellular protein thiols as a cytoprotective mechanism
Arch Biochem Biophys
Dimethoate-induced effects on antioxidant status of liver and brain of rats following subchronic exposure
Toxicology
Protective effects of vitamin E against atrazine-induced genotoxicity in rats
Mutat Res
Dose related induction of rat hepatic drug metabolizing enzymes by diuron and chlorotoluron, two substituted phenyl-urea herbicides
Toxicol Lett
Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats
Toxicology
Glutathione metabolism and its implications for health
J Nutr
Deltamethrin-induced oxidative damage and biochemical alterations in rat and its attenuation by Vitamin E
Toxicology
measurement of atrazine metabolites in human urine after dermal exposure
Anal Chem
Hydroperoxide metabolism in mammalian organs
Physiol Rev
Interactions of organophosphorous insecticides phosphamidon and malathion on lipid profile and acetylcholinesterase activity in human erythorocyte membrane
Indian J Med Res
Effects of organophosphorus insecticide phosphomidon on antioxidant defense components of human erythrocytes and plasma
Indian J Exp Biol
Glucose-6-phosphate dehydrogenase
Atrazine hazards to fish, wildlife, and invertebrates: a synoptic review. US fish and wildlife service
Biol Rep
Role of alpha-tocopherol and beta-carotene in ameliorating the fenvalerate-induced changes in oxidative stress, hemato-biochemical parameters, and semen quality of male rats
J Environ Sci Health B
Biochemical response of bluegill sunfish (Lepomis macrochirus, Rafinesque) to atrazine induced oxidative stress
Bull Environ Contam Toxicol
Serum biochemical and histopathological changes related to the hepatic function in pigs following atrazine treatment
J Appl Toxicol
Oxygen toxicity, oxygen radicals, transition metals and disease
Biochem J
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