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Santosh Rahangadale , Nitin Kurkure , Baijnath Prajapati , Vandana Hedaoo , Arun G. Bhandarkar

Abstract

Male wistar rats (weighting 160-180 g) were divided into six groups of six animals per group. Groups A and F served as control. Groups B, C, D, and E received acrylamide at 20 mg/kg body weight for 28 days and groups C and E received additionally vitamin E (50 IU/kg body weight) for 1 to 28 days and 29 to 42 days of experiment, respectively. The animals from groups A, B, and C were sacrificed on day 28 of experiment and from groups D, E, and F on day 42 of experiment, respectively. The FOB (Functional Observational Battery) and histopathological changes were investigated at the end of 4th week and 6th week. FOB at the end of 4th week, of rats given acrylamide alone, or in combination with vitamin E, revealed a significant change in CNS, neuromuscular, and autonomic domains. A marked decrease in grip strength was recorded. A significant increase in foot splay, reduction in width and angle of sequential stride was noticed. Degenerative changes, necrosis, congestion, and kupffer cell proliferation in liver while vacuolar degenerative changes in tubular epithelium, coagulative necrosis, and hemorrhages in kidney were constant findings in acrylamide intoxicated rats. Neuronal degeneration, severe gliosis, congestion were found in brain. Spinal cord revealed demyelination. Acute microscopic softening of lumbar cord, bilateral necrosis with malacia and liquefaction of white matter, and loss of myelin from grey matter were seen. In the recovery period, vitamin E-treated rats revealed improvement in remyelination of spinal cord. In brain mild gliosis was seen. Thus, it appears that vitamin E is not able to protect them from acrylamide toxicity during active feeding, but after cessation of acrylamide feeding treatment with vitamin E revealed faster recovery as compared to the non-treated group.

Keywords

Acrylamide toxicity, functional observational battery, neurotoxicity, protective effect of vitamin E

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Santosh Rahangadale ¹, Babu Lal Jangir ¹, Manoj Patil ², Trupti Verma ², Arun Bhandarkar ¹, Prashant Sonkusale ¹, Nitin Kurkure ¹

Affiliations
1 Department of Veterinary Pathology, Maharashtra Animal and Fishery Sciences University, Nagpur, Maharashtra, IN
2 Department of Animal Reproduction, Nagpur Veterinary College, Maharashtra Animal and Fishery Sciences University, Nagpur, Maharashtra, IN

Abstract

Male wistar rats (weighting 160–180 g) were divided in six groups of 6 animals per group. Group A and F served as control. Groups B, C, D and E received acrylamide at 20 mg/kg body weight for 28 days and groups C and E received additionally vitamin E (50 IU/kg body weight) for 1 to 28 days and 29 – 42^nd days of experiment, respectively. The animals from groups A, B, and C were sacrificed on day 28th of experiment and from groups D, E, and F on 42^nd day of experiment, respectively. There was significant decrease in the total sperm count and significant increase in the dead sperm count on day 28^th of study due to acrylamide toxicity. At recovery period, there was significant increase in the total sperm count of vitamin-E-treated group of animals as compared to untreated toxicated rats. But, values were significantly lower than control animals. Microscopically, the lesions in the testes of acrylamide intoxicated rats at 28^th day revealed destruction of seminiferous tubules at periphery. No spermatid and spermatocytes were seen in the seminiferous tubules. Detachment of spermatogonial cells started at periphery of seminiferous tubules. Atrophy of seminiferous tubules was a constant finding. Some tubules showed vacuolar degenerative changes in germinal epithelium. During the recovery period, destruction of seminiferous tubules, detachment of spermatogonial cells, and atrophy of seminiferous tubules were observed in group D and E. Few sections revealed only spermatogonial cells. At recovery period vitamin-E-treated rats revealed somewhat better architecture of the seminiferous tubules. Late spermatids were seen in few seminiferous tubules and other revealed starting of spermatogenesis. Thus, it appears that Vitamin E is not able to protect testes from acrylamide toxicity during active feeding, but after cessation of acrylamide feeding treatment with vitamin E revealed faster recovery as compare to not treated group.

Keywords

Acrylamide toxicity, protective effect of vitamin E, testicular toxicity

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