Methyl Parathion-Induced Changes in Free and Protein-Bound SH Levels in Rat Tissues

Abstract

The main objective of this study was to investigate the changes in free and protein-bound SH contents in methyl parathion-exposed rat tissues. The free and protein-bound SH levels are usually affected and depleted by oxidative stress-inducing agents. Results would indicate if methyl parathion toxicity partly results from depletion of sulfhydryl content of tissues. Six-week-old male Wistar albino rats were used in this study. Following exposure to methyl parathion for 3 months, the liver, the brain, and the kidney tissues were removed from the rats. The free and protein-bound SH contents were determined in these tissues. In addition, plasma lactate dehydrogenase levels were determined. Our results showed that methyl parathion exposure significantly lowers the free and protein-bound SH levels in rat tissues. However, lactate dehydrogenase activity in the blood plasma did not display any differences compared to the control group. The free SH concentrations in the control rat liver, brain, and kidney tissues were 3.78 ± 0.1 μmol/100 mg tissue, 1.56 ± 0.08 μmol/100 mg tissue, and 2.16 ± 0.08 μmol/100 mg tissue, respectively, whereas the free SH concentrations in rats exposed to methyl parathion were determined as 0.536 ± 0.1 μmol/100 mg tissue in the liver, 1.06 ± 0.1 μmol/100 mg tissue in the brain, and 0.108 ± 0.03 μmol/100 mg tissue in the kidney. The protein-bound SH concentrations in the liver and in the kidney in rats exposed to methyl parathion displayed a significant decrease also. However, the protein-bound SH level in the brain did not change significantly. These results indicate that methyl parathion exposure partially depletes the free and protein-bound SH levels. Thus, it was concluded that methyl parathion toxicity may partly result from oxidative stress.