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Abstract

The oxidative damage and pharmacokinetics of pendimethalin were studied in male rat. Rats were divided into four groups. To conduct the pharmacokinetic study, the 1st group received a single oral dose of 109 mg pendimethalin /kg body weight and the 2nd group received a single oral dose of corn oil and served as control. To conduct the oxidative damage study, the 3rd group received four oral doses of 109.4 mg/kg b.wt every other day and the 4th group received corn oil as the same manner and served as control. Rats of 1st and 2nd groups were killed after 0.5, 1, 3, 6, 12, 24, 48, 72, 120, and 168 h. Pendimethalin was readily absorbed and subsequently distributed throughout the body. The peak concentrations of the herbicide were reached in serum, liver and kidney at 12 h and in brain at 24 h following administration. The compound begins to decline in all tissues as time passed. Pendimethalin was disappeared biexponentially from serum, liver, kidneys and brain. The terminal half-life t½ of pendimethalin was 14.0, 15.0, 2.5, and 29.0 h for the serum, liver, brain and kidneys, respectively. At termination of 168 h, the urinary and fecal cumulative excretion rose to 23.81 and 71.21%, respectively. Rats of 3rd and 4th groups were killed 24 h after the last dose. Exposure of rats to pendimethalin caused a significant increase in tissue MDA, LDH and ALP levels as compared to controls. The activities of catalase (CAT) in serum, liver and kidney were significantly increased, while brain CAT activity was significantly decreased due to pendimethalin treatment. Our results indicated that there was no tendency for pendimethalin to retain in rat tissue. The results also showed that pendimethalin exposure had profound influence on the oxidative stress markers and enzyme activities of the exposed male rat and these enzymes can be used as biomarkers in determining pendimethalin toxicity.