Paclitaxel-induced neuropathic pain (PINP) is a dose-limiting side effect that largely affects the patient’s quality of life and may limit the use of the drug as a chemotherapeutic agent for treating metastatic breast cancer and other solid tumors. Recently, a putative role for the gaseous mediator hydrogen sulfide (H2S) in nociception modulation has been suggested. The aim of the present study was to investigate the potential efficacy of a slow release H2S donor to alleviate and prevent PINP. The H2S donor enhanced paclitaxel’s anti-proliferative effects against the breast cancer cell line MCF-7, suggesting that it alleviates paclitaxel-induced thermal hyperalgesia, via KATP channels. It also prevents PINP possibly by blocking the paclitaxel-induced reduction in the generation of H2S, in the tissues, while enhancing the anti-cancer activity of paclitaxel.
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