title: Antioxidant defenses and lipid peroxidation in the cerebral cortex and hippocampus following acute exposure to malathion and/or zinc chloride.
abstract: This study investigates the effects of acute exposure to organophosphate insecticide malathion (250 mg/kg, i.p.) and/or ZnCl2 (5 mg/kg, i.p.), with the following parameters: lipid peroxidation and the activity of acetylcholinesterase (AChE), glutathione reductase (GR), glutathione S-transferase (GST), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PDH), and the levels of total glutathione (GSH-t) in the hippocampus and cerebral cortex of female rats. Malathion exposure elicited lipid peroxidation and reduced AChE activity in the cerebral cortex and hippocampus. It also reduced the activity of GR and GST, and increased G6PDH activity in the cerebral cortex, without changing the levels of GSH-t and GPx activity. ZnCl2 exposure reduced AChE activity and caused a mild pro-oxidative effect, since lipid peroxidation was increased in the hippocampus. ZnCl2, individually or in combination with malathion, caused a reduction in GR and GST activity in the cerebral cortex. Malathion and/or ZnCl2 did not change the GSH-t levels. Moreover, ZnCl2 prevented the increase in G6PDH activity caused by malathion. It showed that ZnCl2 had little effect against the changes induced by malathion. In fact, zinc itself produced pro-oxidant action, such as the reduction in the activity of the antioxidant enzymes GR and GST.
authors.affiliation: Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, SC 88040-900, Florianópolis, Brazil.
authors.forename: Patrícia S
authors.initials: PS
authors.lastname: Brocardo
authors.forename: Pablo
authors.initials: P
authors.lastname: Pandolfo
authors.forename: Reinaldo N
authors.initials: RN
authors.lastname: Takahashi
authors.forename: Ana Lúcia S
authors.initials: AL
authors.lastname: Rodrigues
authors.forename: Alcir L
authors.initials: AL
authors.lastname: Dafre
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D002712:Chlorides / Q000494:pharmacology*; D002800:Cholinesterase Inhibitors / Q000633:toxicity*; D005260:Female; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008294:Malathion / Q000037:antagonists & inhibitors / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis / Q000378:metabolism; D017967:Zinc Compounds / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D002712:Chlorides; D002800:Cholinesterase Inhibitors; D017392:Thiobarbituric Acid Reactive Substances; D017967:Zinc Compounds; C016837:zinc chloride; D005954:Glucosephosphate Dehydrogenase; D005979:Glutathione Peroxidase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D000110:Acetylcholinesterase; D005978:Glutathione; D008294:Malathion