Abstract
Aim: Endosulfan is an important toxic agent which generates free oxygen radicals in liver. In Cukurova region, some relation between the incidence of toxic injury to liver and widespread use of endosulfan has been suggested. Since endosulfan is a frequently used pesticide, it was planned to investigate whether endosulfan could do liver injury and increase lactic dehydrogenase in liver. Methods: Sixty mature (30 controls, 30 experimental) Mus musculus, weighing between 23-40 g, obtained from Medical Experimental Surgery Research Center of Cukurova University, were utilized in this study. The effects of oral administration of endosulfan (0.24 mg per 100 g body weight) daily for 90 days (short term) and 180 days (long term) were investigated. Results: At the end of the experimental period, no effect on body weights but an increase on liver weight and hepato/somatic index were observed in both short and long terms. On microscopic examination, livers of experimental groups exhibited severe damage histopathologically. On the other hand, livers of the same group, particularly in long term oral endosulfan administered mice, demonstrated some toxic changes and high levels of lactic dehydrogenase activity with enzyme histochemical method. Conclusion: The exposure to endosulfan in mice caused liver tissue damage histologically, this was also demonstrated by hepatic/somatic index and increased levels of liver LDH assesed with histochemical method.
Highlights
Endosulfan is an important environmental pollutant which is a pesticide of organochlorine
The exposure to endosulfan in mice caused liver tissue damage histologically, this was demonstrated by hepatic/somatic index and increased levels of liver Lactic dehydrogenase (LDH) assesed with histochemical method
Even though endosulfan had no significant effect on total body weight of mice (p>0.05), it increased the weight of livers and hepato/somatic index (HSI: liver weight/body weight) significantly (Table 1)
Summary
Endosulfan is an important environmental pollutant which is a pesticide of organochlorine. Primary site of organochlorine storage in the body is adipose tissue. It is metabolized in the liver as a lipophilic xenobiotic to hepatotoxic intermediates by monooxygenase systems which cause oxidative stress [1]. Free radicals generated during oxidative stress cause lipid peroxidation of cell membranes which is in turn prevented by antioxidant enzymes [2,3,4]. Endosulfan alters the activities of lactic dehydrogenase, glucose-6-phosphate dehydrogenase and alkaline phosphatase, and decreases mitochondrial energy production in mice [5]. Lactic dehydrogenase (LDH; 1.1.1.27) is a hydrogen transferring enzyme that catalyzes
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