Capsaicin is a principal pungent ingredient of red chili peppers, first isolated in the early nineteenth century by Christian Friedrich Bucholz. Widely consumed as a spice in South Asia and Latin America, Capsaicin has been used to treat pain and inflammation associated with a variety of diseases, including rheumatoid arthritis, diabetic neuropathy, post-masectomy pain, cluster headaches, and herpes zoster. Although recent studies have evaluated capsaicin as a novel anti-cancer agent, and mechanisms of capsaicin in preventing cancer have been described sporadically, the literature lacks a comprehensive review of capsaicin as a chemo-preventive agent. Role of Capsaicin in Oxidative Stress and Cancer offers a thorough exploration of the preventive and therapeutic effects of capsaicin in cancer models such as melanoma, pancreatic cancer, colon cancer, gastric cancer, breast cancer, prostate cancer, skin cancer, lung cancer, multiple myeloma and glioma. The contributors, all internationally recognized researchers, identify various molecular and cellular targets of capsaicin, and show the critical role of mitochondria in capsaicin-mediated therapeutic effects. Readers will learn how capsaicin prevents or may treat cancer, how different cells respond to capsaicin, how environmental carcinogen-induced carcinogenesis can be prevented by capsaicin and the mechanism of oxidative stress caused by capsaicin. This book will benefit medical students, oncologists and cancer researchers everywhere.

This book describes the mechanism of the anti-cancer effects of capsaicin including the involvement of cytochrome P-450 in the bioactivation; identification of mitochondria as the key target site for oxidative stress; involvement of mitochondrial respiratory chain in the production of ROS; prevention of chemically-induced carcinogenesis, discussion on TRPV-1 receptor mediated or independent anti-cancer effects; identification of p53 activation as a possible mechanism; involvement of Cox-2 in apoptosis, suppression of transcription factors such as NF-kB and STAT-3; inhibition of cell survival pathways including PI3K/Akt and the involvement of intrinsic mitochondrial cell death pathway.