Green tea extract administration protects against the nephrotoxicity induced by gentamycin and amikacin in rats

Despite their beneficial effects, aminoglycosides including gentamycin [GEN] and amikacin [AK] have considerable nephrotoxic side effects. This study investigaged the effects of green tea [GT] extract on biochemical and morphological kidney damage induced by GEN and AK in rats. Sixty male albino rats were used in this study and divided into 6 groups each contains ten rats. The first group was the control group injected with 0.4 ml saline. Each rat of the second group was given 12.5 ml of green tea extract [3%] twice daily to drink it orally for 25 days. The 3[rd] group received GEN [80mg/kg] once daily intraperitoneally for 10 days. The 4[th] group was administered AK [180 mg/kg] once daily intraperitoneally for 10 days. The 5[th] group received GT extract for 15 days then concomitant with GEN for 10 days. The 6[th] group received GT extract for 15 days then concomitant with AK for 10 days. GEN and AK groups showed significant increase in serum urea and creatinine [Cr] which was significantly decreased in green tea consuming rats before GEN and AK administration. GEN and AK treated rats showed significant decrease in the activity of calalase enzyme and reduced glutathione level in kidney tissues which were significantly increased in GT consuming rats prior to GEN and AK injection. Light microscopic examination of kidney tissues of GEN and AK groups revealed tabular necrosis and degenerative changes which were modulated by the consumption of green tea prior to GEN and AK administration. In conclusion green tea ameliorates and modulates GEN and AK induced-nephrotoxicity and oxidative damage by enhancing the antioxidant defense system

Determination of postmortem fluoxetine concentration in blood, liver, hair and in different regions of brain of albino rats

Fluoxetine is a selective serotonin reuptake inhibitor [SSRI]. Measurements of postmortem levels of the drug are helpful to demonstrate its usefulness in. forensic toxicology. For this reason, a rapid and sensitive high- pressure liquid chromatographic method has been developed for determination of the antidepressant fluoxetine in postmortem samples for 50 rats given intraperitoneal fluoxetine hydrochloride at the therapeutic levels. The postmortem samples were including blood, hair, liver, and discrete brain regions [raphenucleus, hypothalamus, and brain striatum].Fifty rats weighing from 200-250 gm. Rats were divided into 5 groups 10 rats per each group: group [1] was given ordinary rat diet, group [2] received 1ml/kg distilled water, group [3] was given fluoxetine hydrochloride once at a dose of 20mg/kg 30 minutes before killing and collection of samples, group [4] was given 10mg/kg fluoxetine hydrochloride once daily for 15 days and killed 30 minutes after the last dose, group [5] was given 10mg/kg. fluoxetine hydrochloride once daily for 9 days then killed on the 10th day after 30 minutes of 20mg/kg fluoxetine hydrochloride. Rats were sacrificed by decapitation and samples were collected immediately after death. In group III, the highest postmortem levels were observed in the raphenucleus followed by brain striatum, then the blood. In group IV, the highest postmortem levels were in hair followed by raphenucleus, then striatum followed by the liver. Meanwhile, in Group V, hair showed the highest postmortem levels followed by brain striatum then raphenucleus and lastly the liver. In conclusion, while blood is still the preferred matrix to link concentration and effect, analysis of hair, liver, and brain tissue can provide additional valuable information, not only in pure overdose cases

effect of vitamin E administration on cisplatin-induced oxidative and histopathological damage of kidney, liver and lens tissues in albino rats

Cisplatin is one of the most active cytotoxic agents in the treatment of cancer but its clinical use is associated with toxicity. The present study evaluated biochemically and histologically the effect of vitamin E as a line of prevention of cisplatin toxicity in rats. Its was carried out on 90 adult male albino rats divided into 6 groups each contains 15 rats, the first group was used as-ve control, the second group received distilled water 1ml/animal intraperitoneally [IP], the third group received corn oil 0.25 ml/animal orally,the fourth group received vitamin E 100 mg/kg orally. Animals of groups II, III and IV served as +ve controls. The fifth group received cisplatin 5 mg/kg IP and the sixth group received vitamin E 100 mg/kg orally 24 hours prior to IP cisplatin 5 mg/kg. After 7 days of treatment, rats were sacrificed,then Malondialdehyde [MDA], reduced glutathione and glutathione perioxidase were measured in kidney, liver and lens tissues. Also kidney, liver and lens tissues were prepared for light microscopic examination. The results revealed significant increase in kidney, liver and lens MDA levels in rats treated with cisplatin in comparison to the-ve control group. Reduced glutathione and glutathione perioxidase levels in kidney, liver and lens were significantly lower in cisplatin group than in the-ve control group. Histopathological examination revealed renal and liver necrosis and cataract changes in cisplatin treated rats. The increased MDA levels, the decreased antioxidant enzymes and histopathological damage in the kidney, liver and lens of rats administered cisplatin were significantly improved with vitamin E administration. So, it is concluded that, vitamin E may play a role in preventing cisplatin induced nephrotoxicity, hepatotoxicity and cataract formation in cancer patients