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Dichloroacetic acid-induced testicular toxicity in male rats and the protective effect of date fruit extract.
BMC Pharmacology & Toxicology 2017 April 23
BACKGROUND: The present study was designed to investigate the protective effect of aqueous date extract (ADE) against the dichloroacetic acid (DCA)-induced testicular injury in rats.
METHODS: Forty-eight male Wistar rats were randomly divided into six groups of eight: group I served as the control; group II was given ADE (4 ml/kg) by gavage; groups III and IV received DCA at 0.5 and 2 g/L drinking water, respectively; and groups V and VI received DCA at 0.5 and 2 g/L drinking water, respectively, before ADE administration. The experiment was performed for two months.
RESULTS: Results showed that the absolute weights of testes and epididymis were decreased following the DCA administration. The testosterone, FSH and LH levels were also decreased. Severe histopathological changes in testes were observed including degeneration of seminiferous tubules and depletion of germ cells. These changes were associated with alterations of oxidative stress markers. Levels of lipid peroxidation and SOD and CAT activities were increased, while activity of GPx and GSH levels were decreased. Pretreatment with ADE has effectively alleviated the oxidative stress induced by DCA thereby restoring these parameters to normal values.
CONCLUSIONS: These results suggest that ADE has a protective effect over DCA-induced oxidative damage in rat testes.
METHODS: Forty-eight male Wistar rats were randomly divided into six groups of eight: group I served as the control; group II was given ADE (4 ml/kg) by gavage; groups III and IV received DCA at 0.5 and 2 g/L drinking water, respectively; and groups V and VI received DCA at 0.5 and 2 g/L drinking water, respectively, before ADE administration. The experiment was performed for two months.
RESULTS: Results showed that the absolute weights of testes and epididymis were decreased following the DCA administration. The testosterone, FSH and LH levels were also decreased. Severe histopathological changes in testes were observed including degeneration of seminiferous tubules and depletion of germ cells. These changes were associated with alterations of oxidative stress markers. Levels of lipid peroxidation and SOD and CAT activities were increased, while activity of GPx and GSH levels were decreased. Pretreatment with ADE has effectively alleviated the oxidative stress induced by DCA thereby restoring these parameters to normal values.
CONCLUSIONS: These results suggest that ADE has a protective effect over DCA-induced oxidative damage in rat testes.
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