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Amethopterin is used as a chemotherapeutic agent, and its antioxidant activity is used to treat many cancer types. This study aimed to study the ameliorating effect of L-carnitine against amethopterin-induced cardiac injury and oxidative stress in male rats. Sixty male albino rats were equally divided into six groups; the first and second groups were the control and L-carnitine groups, respectively, while the third group was treated with amethopterin rat group; the fourth and fifth groups were co-treated and post-treated with amethopterin rat with L-carnitine, respectively, and the sixth group was self-treated with amethopterin rat group. Cholesterol, triglycerides, low-density lipoprotein (LDL), glutathione, and total protein levels in amethopterin group showed a significant decrease when compared with control group, while high-density lipoprotein (HDL), glutamic oxaloacetic transaminase (GOT), malondialdehyde (MDA), catalase, and nitric oxide (NO) levels in amethopterin group showed a significant increase when compared with control group. Cholesterol, triglycerides, LDL, GOT, MDA, and catalase levels in the self-treated group showed a significant increase when compared with amethopterin group, while glutathione, total protein, and NO levels in the self-treated group showed significant decrease when compared with amethopterin group. Many of abnormalities as moderate hydrophobic changes of myofibrillar structure with striations, myocardial atrophy, cytoplasmic vacuoles, edema, and leukocyte infiltration were detected in cardiac tissues in amethopterin rat group. A significant increase of the apoptotic protein p53 and CD68 immunoreactivity, despite a significant decrease in the antiapoptotic Bcl–2 proteins after amethopterin injection when compared with control group, was observed. Treatment (co and post) with L-carnitine improved the biochemical, histopathological, and immunohistochemical alterations in the heart treated with amethopterin.

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Vitamin B17 (VB17), also known as amygdalin and laetrile, is a type of carbohydrate occurring naturally in many plants, such as apricot kernels which have obtained a great interest in cancer therapy. This study aimed to investigate the hepatic protective potential of VB17 against Ehrlich ascites carcinoma (EAC)–bearing mice-induced liver injury, DNA damage, apoptotic P53, and PCNA alterations. A total of 100 female mice were divided into 5 groups (1st group, control group; 2nd group, VB17 group; 3rd group, EAC group; 4th group, pre-treated EAC with VB17; 5th group, co-treated EAC with VB17). Results showed that the presence of VB17 in pre-treated and co-treated groups lead to decreased DNA damage, microsomal protein, NADPH cytochrome c reductase, alpha-fetoprotein (AFP), AST, ALT, and ALP while showed increased cytochrome b5, cytochrome P450 amidopyrine N-demethylase, and aniline 4-hydroxylase compared with the EAC group. Many histopathological changes were observed in liver sections in EAC as moderate fibrosis and marked diffuse necrosis of hepatic tissue, marked inflammatory cells, and congested blood sinusoids. On the other hand, there was a moderate degree of improvement in hepatocytes in liver sections in pre-treated VB17+EAC, while a mild degree of improvement in hepatocytes, moderate cellular infiltrations, and moderate cytoplasmic vacuolization of hepatocytes in liver sections in co-treated EAC+VB17. In addition, there was a depletion in hepatic P53 and PCNA protein expression compared with the EAC group. It could be concluded that VB17 has a potential hepatoprotective effect against EAC cell–induced liver toxicity.

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