ABSTRACT
Conclusion:
Acute exposure to malathion disrupts the oxidant-antioxidant balance and causes oxidative stress in kidneys.
Results:
ChE activities decreased, TOS levels and TNF- α levels increased in all experimental groups compared with control group (p'<0.05). AGEs levels of the high dose group elevated significantly compared with control and group 3 (p'<0.05). SOD levels of group 3 and 4, and MDA levels of group 3 showed an increase compared with control group, however this did not reach statistical significance (p'=0.054). PON1-ARE levels diminished in group 3 and 4 compared with control (p'<0.05). AOPP levels did not change significantly (p'=0.735).
Methods:
Four groups (n=6) were designed to evaluate the effects of different doses of acute malathion exposure on rat kidney. Control group was given only corn oil. Malathion dissolved in corn oil was administered to Group 2 (100 mg/kg), Group 3 (200 mg/kg) and Group 4 (400 mg/kg) via oral gavage. The rats were sacrificed after 24 hours and renal tissue supernatants are analyzed to determine cholinesterase (ChE) activity, total oxidant status (TOS), TNF-α, advanced glycation end products (AGEs), advanced oxidation protein products (AOPP), superoxide dismutase (SOD) activity, malondialdehyde (MDA), and paraoxonase 1-arylesterase activity (PON1-ARE).
Objective:
Pesticides have been used in agriculture to enhance food production by eradicating undesired insects and controlling disease vectors. Malathion is one of the most widely used organophosphate pesticides. However, it has been postulated that organophosphate pesticides lead to oxidative stress through formation of excessive reactive oxygen species and disrupting the antioxidant defense systems.Objective: Pesticides have been used in agriculture to enhance food production by eradicating undesired insects and controlling disease vectors. Malathion is one of the most widely used organophosphate pesticides. However, it has been postulated that organophosphate pesticides lead to oxidative stress through formation of excessive reactive oxygen species and disrupting the antioxidant defense systems.