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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
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.
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This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
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.