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Effects of Vanadium Pentoxide on the Histological and Sperm Parameters of Male Guinea Pigs
Abstract
The pharmacological effects of intraperitoneal administration of different doses of vanadium pentoxide (V2O5) on the histological and sperm parameters of male guinea pigs were investigated. Also investigated
were the effects of oral pretreatment with different doses of vitamin E (a known protein kinase C inhibitor) on the V2O5 -induced responses of the testis and liver of male guinea pigs. In n = 5 experiments, vanadium pentoxide in the dose range of 4.5-12.5mg/kg caused destruction of the testicular and liver architecture. This was characterized by a
reduction in spermatogonia, destruction of seminiferous tubules, necrosis of the testicular tissues, necrosis of liver cells, fatty cells infiltration and vacoulation. Oral administration/ pretreatment with vitamin E in the dose range of 500-2000I.U caused a reversal of the vanadium pentoxide –induced histological damages of the testis and the liver cells. Furthermore, in n = 5 animals experiments, Vanadium pentoxide (4.5-12.5 mg/kg/) caused a statistically significant increase in the percentage basal cell death, from 5.0 to 75.0 ± 1.0%, reduction in sperm motility from 90.0 to 31.0 ± 3.9%, reduction in sperm count from 80.0 x106cells/ml to 25.0± 4.0 x 106cells/ml and alteration in the spermatic cell morphology ( i.e. causing a change in the cellular structure of sperm cells and an increase in abnormal cells count) of the male guinea pigs. These inhibitory effects were significant at P < 0.05 (ANOVA). These effects were all dose- and time-dependent and may have a role in oxidative pathology of vanadium pentoxide.
were the effects of oral pretreatment with different doses of vitamin E (a known protein kinase C inhibitor) on the V2O5 -induced responses of the testis and liver of male guinea pigs. In n = 5 experiments, vanadium pentoxide in the dose range of 4.5-12.5mg/kg caused destruction of the testicular and liver architecture. This was characterized by a
reduction in spermatogonia, destruction of seminiferous tubules, necrosis of the testicular tissues, necrosis of liver cells, fatty cells infiltration and vacoulation. Oral administration/ pretreatment with vitamin E in the dose range of 500-2000I.U caused a reversal of the vanadium pentoxide –induced histological damages of the testis and the liver cells. Furthermore, in n = 5 animals experiments, Vanadium pentoxide (4.5-12.5 mg/kg/) caused a statistically significant increase in the percentage basal cell death, from 5.0 to 75.0 ± 1.0%, reduction in sperm motility from 90.0 to 31.0 ± 3.9%, reduction in sperm count from 80.0 x106cells/ml to 25.0± 4.0 x 106cells/ml and alteration in the spermatic cell morphology ( i.e. causing a change in the cellular structure of sperm cells and an increase in abnormal cells count) of the male guinea pigs. These inhibitory effects were significant at P < 0.05 (ANOVA). These effects were all dose- and time-dependent and may have a role in oxidative pathology of vanadium pentoxide.
