By Kartick C. Pramanik (auth.), Sanjay K. Srivastava (eds.)
This booklet describes the mechanism of the anti-cancer results of capsaicin together with the involvement of cytochrome P-450 within the bioactivation; id of mitochondria because the key goal web site for oxidative rigidity; involvement of mitochondrial respiration chain within the creation of ROS; prevention of chemically-induced carcinogenesis, dialogue on TRPV-1 receptor mediated or self sustaining anti-cancer results; id of p53 activation as a potential mechanism; involvement of Cox-2 in apoptosis, suppression of transcription components resembling NF-kB and STAT-3; inhibition of phone survival pathways together with PI3K/Akt and the involvement of intrinsic mitochondrial telephone demise pathway.
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Additional info for Role of Capsaicin in Oxidative Stress and Cancer
Vanilloid-containing botanical products have been used as medicinal agents since antiquity (Szallasi and Blumberg 1999). For instance, oral solutions containing red pepper powder are employed as a traditional remedy for gastrointestinal illnesses in South African’s populations (Snyman et al. 2001). In the modern medicine, CPS formulations are used topically to treat a variety of diseases associated with neurogenic pain and inflammation (Bırò et al. 1997), and both CPS and RTX are currently under evaluation in clinical trials for various pathological conditions (Appendino and Szallasi 1997; Szallasi and Blumberg 1999).
Apoptosis can be triggered in the absence of FasL by overexpression of the Fas cytoplasmic domain or a Fas receptor lacking the N-terminal 42 amino acids (Papoff et al. 1999). The intracellular death domains of DRs show a high tendency to self-associate, and when overexpressed by gene transfer in eukaryotic cells trigger apoptotic signaling (Boldin et al. 1995). In this regard, we have firstly underlined an important role for ligand-independent Fas/CD95 clustering and activation of ATM/p53 pathway in CPS-dependent TRPV1-mediated apoptosis of UC cells (Amantini et al.
CPS treatment initiated a rapid increase in [Ca2+]i, and caused apoptosis in transformed human Jurkat T cells (Macho et al. 1999) and human glioblastoma cells (Lee et al. 2000) in a TRPV1-independent manner. However, in later case [Ca2+]i was not believed to be the stimulus that triggered apoptosis in glioblastoma cells, and it has been suggested that the CPS-induced rapid rise of [Ca2+]i may be the result of a nonspecific disruption of the plasma membrane (Meddings et al. 1991; Lee et al. 2000).
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