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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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R. Mahaprabhu ¹, A. G. Bhandarkar ¹, Babu Lal Jangir ¹, S. P. Rahangadale ¹, N. V. Kurkure ¹

Affiliations
1 Department of Pathology, Nagpur Veterinary College, Maharashtra Animal and Fishery Sciences University, Nagpur - 440 006, IN

Abstract

An ameliorating effect of Ocimum sanctum on the toxic effect of meloxicam, a new non-steroidal anti-inflammatory drug was studied by evaluating haemato-biochemical parameters, oxidative stress, gross and histopathological changes in various organs of Wistar rats. A total of thirty-six male rats were divided in six experimental groups each comprising of six rats and numbered from G₁ to G₆. Meloxicam toxicity was induced by oral feeding of meloxicam at 1.2 mg/kg and 2.4 mg/kg body weight in G₂ and G₃ respectively for 28 days. Group G₄ and G₅ were fed with 1.2-mg/kg body weight and 2.4-mg/kg body weight of meloxicam along with 200 mg/kg body weight of aqueous extract of Ocimum sanctum. Group G₁ serve as control while group G₆ was kept as treatment control and fed only aqueous extract of Ocimum sanctum at 200 mg/kg body weight. Clinical finding showed mild diarrhea from 23^rd day onwards in-group treated with 2.4-mg/kg body of meloxicam. Significant reduction of hemoglobin and packed cell volume (PCV) was observed in both the group treated with 1.2 mg/kg and 2.4-mg/ kg body wt. of meloxicam. Ocimum sanctum could restore the hemoglobin and PCV value in-group treated with meloxicam at low dose level. Serum alkaline phosphatase, serum glutamic pyruvic transaminase, Serum glutamic oxaloacetic transaminase and total bilirubin were found elevated in meloxicam treated groups and indicated hepatotoxic activity of meloxicam. Ocimum sanctum could reduce hepatotoxic activity of meloxicam in group G₄ receiving meloxicam at lower dose rate along with Ocimum sanctum failed to regulate creatinine level in meloxicam treated groups. In meloxicam toxicity elevated Lipid peroxidation values was noticed in liver and kidneys, while superoxide dismutase and glutathione did not revealed any change. Stomach and intestine revealed hemorrhagic gastroenteritis and ulcers. Perivascular necrosis with infiltration with inflammatory cells was evident in liver. Interstitial nephritis, myocardial necrosis and spongiform encephalopathy were important lesions. The Ocimum sanctum could only counteract the toxic effect of meloxicam in liver and gastrointestinal tract.

Keywords

Meloxicam toxicity, Ocimum sanctum, oxidative stress, Wistar rats

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