The aim of the present investigation was to study the toxic influences of taxol (TXL) on the testes of rats and the protective impact of melatonin (MLT) against such effects. Rats were classified into control, sham, TXL, MLT, and MLT+TXL-treated groups. Histological and ultrastructural changes were observed in testicular tissues of TXL-intoxicated rats including thickening of tunica albuginea and degenerative alterations in spermatogenic, Sertoli, and Leydig cells. A significant increase (Pp0.05) was found in the thickness of tunica albuginea and numbers of tubules without sperm, apoptotic germinal epithelia, and apoptotic Leydig cells, whereas the diameter of tubules and height of germinal epithelia displayed a significant decrease (Pp0.05) compared with the control, sham, and MLT-treated groups. Immunohistochemically, a marked decrease (Pp0.05) in Bcl-2 immunoreactivity and significant elevation (Pp0.05) in P53 and caspase-3 immunoreactivities were recorded. Co-treatment of MLT and TXL modulated such histological, histomorphometrical, and ultrastructural changes induced by TXL. Also, MLT had a protective effect against testicular apoptosis induced by TXL, as shown by the elevated expression of Bcl-2 and decreased expression of P53 and caspase-3. In conclusion, the current investigation proved that MLT had a protective role against TXL-induced testicular cytotoxicity, which may be a result of inhibition of testicular apoptosis.
Cancer is a worldwide growing health problem caused expanding utilization of chemotherapy which is still the most popular and first-line method of treating malignancies. The current study aimed to use histological, histomorphometrical, immunohistochemical, and ultrastructural protocols to evaluate the hepatotoxic effect of Taxol (TXL) and the ameliorative influence of melatonin (MLT) against toxic impacts in the liver of adult rats. Fifty rats were used and randomly divided into four groups: control, sham, TXL (7.5 mg kg 1 i.p.), MLT (10 mg kg -1 i.p.) and MLT+TXL (10 mg kg -1 + 7.5 mg kg -1 i.p.) groups. The results indicated the presence of numerous histopathological, histomorphometrical, and ultrastructural changes in the hepatic tissues of TXLtreated animals including destruction of the normal building of the hepatic lobules, with marked decline in the number of intact hepatocytes, and a rise in the number of necrotic hepatic cells, centrilobular and periportal inflammatory cells, and degraded Kupffer cells, in addition to noticeable apoptosis which was represented immunohistochemically by marked elevation in P53 and casapase3 (Cas3), and diminution in Bcl-2 immunoreactivities. Also, strong CD163 immunoreactivity was seen in TXL-treated rats. Nevertheless, co-administration of MLT with TXL reversed most of the histological and ultrastructural alterations triggered by TXL in rats. Moreover, MLT revealed a diminished effect against liver apoptosis and inflammation caused by TXL which was represented by elevation of immunoexpression of Bcl-2 and decreased immunoexpression of P53, Cas3, and CD163. In Conclusion, the present study proved that MLT has ameliorative impact against TXL-triggered hepatic toxicity through its antioxidant, anti-inflammatory and anti-apoptotic properties.
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