In addition to that, the quinone metabolite of ETP has enhanced antitumour activity and oxidising ability than its parent drug. This impairment of DNA replication activates a cascade of events that eventually leads to cell death via apoptosis. ETP exerts its cytotoxic effect by impairing the activity of topoisomerase II enzyme which eventually results in single- and double-stranded DNA breaks during DNA replication. Yet, the clinical use of ETP is often limited due to its toxic effects on organs including liver, kidney, heart and lungs. It is used alone or in conjugation with other antineoplastic drugs against a wide variety of malignancies. Įtoposide (ETP) is a semisynthetic derivative of podophyllotoxin and one of the leading antitumour agents in cancer chemotherapy. Therefore, new therapies are constantly being developed and searched for in order to minimise the life-threatening side effects of the current anticancer drugs without affecting their efficacies. However, these drugs cannot differentiate between cancer cells and normal cells leading to off-target toxicities. Chemotherapeutic drugs are cytotoxic agents that stop the abnormal growth of cancerous cells.
Taurine effects on clotting license#
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.ĭespite advances in developing new anticancer drugs, and a continuous increase in the number of cancer survivors, the off-target toxicity of anticancer drugs that eventually affects the quality of life is the main challenge facing oncologists. Publication costs for this article were supported by ecancer (UK Charity number 1176307).Ĭopyright: © the authors licensee ecancermedicalscience. Keywords: etoposide, toxicology, immunohistochemistry, brain, glial fibrillary acidic protein We concluded that co-treatment with vinpocetine could serve as a complementary therapeutic agent in reducing brain injury and toxicity induced by ETP. Co-treatment with taurine, piracetam and vinpocetine counteracted ETP-induced brain injury and altered serum biomarkers levels. Moreover, ETP treatment resulted in upregulation of glial fibrillary acidic protein expression and histopathological alterations in the rats’ brain compared to the control group. Administration of ETP reduced body weight significantly, enhanced production of serum proinflammatory cytokines including tumour necrosis factor-alpha, interleukin-1 beta (IL-1β) and IL-6 and decreased glutathione serum levels. A total of 30 female albino rats were equally divided into five groups the 1 st and 2 nd groups were the control and ETP-treated groups, respectively, while the 3 rd, 4 th and 5 th groups were ETP-treated rats cotreated with taurine, piracetam and vinpocetine, respectively. The current research investigates the protective potential of taurine, piracetam and vinpocetine on serum biomarkers associated with inflammation and brain injury induced by ETP in a rodent model. Many studies have reported on ETP-induced peripheral neuropathy however, few reports have focused on its brain toxicity. Etoposide (ETP) is one of the leading antitumour agents in cancer chemotherapy.
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