Oral Supplementation of ?-Carotene Significantly Ameliorates Testicular Oxidative Stress in the Streptozotocin-Diabetic Rat

Authors

  • B Shrilatha
  • BM Thyagaraju
Abstract:

Background Our recent findings have shown that the rat testis is subjected to significant oxidative stress during the early phase of diabetes induced by Streptozotocin (STZ). In the present study, we have investigated whether oral supplementation of β-carotene (BC) to pubertal rats would provide protection against diabetes associated oxidative stress in testis and liver. MaterialsAndMethods Male (6 wk old) rats were rendered diabetic by an acute dose of Streptozotocin (60 mg/kg bw) and were given oral BC supplements (20 mg/kg bw/d on alternate days) for 4 weeks. The modulatory potency of BC was assessed by determination of selected markers of oxidative stress in testis and liver. Results The testis of STZ-administered rats exhibited significantly elevated status of lipid peroxidation (cytosol and mitochondria) and increased ROS production compared to the non-diabetic controls. Oral supplements of BC completely normalized the oxidative damage in testis. Further, STZ-induced depletion of reduced glutathione (GSH) and elevated protein carbonyl content in testis were also restored to normalcy. The protective effects of BC in testis were also discernible in terms of restoration of activities of various antioxidant enzymes in diabetic rats. Furthermore, STZ-induced oxidative impairments in liver were also abrogated significantly by BC treatment. STZ-induced perturbations in serum and testicular lipid profiles in diabetic rats were also attenuated by BC treatment. Conclusion Collectively, our data indicate that oral supplementation of β- carotene can significantly mitigate the diabetes associated oxidative impairments in testis as well as in liver and suggest its efficacy as a complementary therapeutic agent in the management of diabetes associated oxidative stress mediated complications.

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Journal title

volume 2  issue 2

pages  74- 81

publication date 2008-02-01

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