I desired to learn out from the oncologist working particularly on NAC like antioxidant and cancer. My query is related to NAC, since Jan 2014, Nature news published an article entitled "Antioxidants speed cancer in mice" by Ledford also supported by some others articles too like Sayin et al., “Antioxidants accelerate lung cancer progression in mice,” Science Translational Medicine, 6: 221ra15, 2014 and two more articles, however several studies in decades showed the chemopreventive as well as anti cancerous effects of NAC, which it puts in clinical trials. Is it true to conclude like antioxidant cause more harms in cancer than beneficial effects as raised by Andy Coghlan and other also. How do you look this?
There is evidence that NAC prevents zeta chain cleavage on T-cell receptors, preventing one maneuver of tumor to evade immunological surveillence. Ichim, T, et al.
Thanks Dr. Rodrigo for concern of my query. yes I agree that homeostasis of oxidative stress in tumor cell greatly matter for the survival in death of tumor. new concept related antioxidant showed the higher scavenging power of these molecule even induce in tumor growth. I desire to know whether the antioxidant level of blood sera can be correlated directly with Ros concentration in tumor micro environment. If it is true all concept of chemoprevention and uses of some photochemical in sometime therapy fails.
Shankar:
It is well known that antioxidants are associated with a checkered history in the broad context of their purported potentialities in the chemoprvention of cancer or treatment. Recently, it was reported that the dietary antioxidants, N-acetyl-L-cysteine (NAC) and vitamin E hastened the progression of lung tumorigenesis in mice. Antioxidant activity (AA) is a chemical or molecular property of a compound. Molecules with AA activity can impair the levels of reactive oxygen and nitrogen species (ROS and NOS) in cells. However they also can accentuate the proliferation rate of cancer cells. The consequences are increased tumor burdens and attenuated survival. Impaired expression of the tumor suppressor gene protein, p53, can evoke higher rates of cellular proliferation. Neither NAC and nor vitamin E influenced tumor growth in mice that did not possess p53.
A role for ROS in promoting cell motility during stress situations in leukocytes has been recently reported; treatment with NAC mitigated the increased enhanced, stress-induced migration potential of bone marrow leukocytes.
The capacity for apoptosis induction by the ROS generator (ATO), arsenic trioxide (As2O3), in MCF-7 cancer cells was reported to be inversely correlated with the cellular levels of GSH (glutathione), a major intracellular antioxidant in mammalian cells. NAC, a precursor of GSH, is efficiently transported into cells unlike GSH. Impeding cancer cell DNA replication and repair and the induction of oxidative stress by the inhibition of both GSH and thioredoxin (Trx) systems have been advanced as cancer chemotherapeutic strategies.
The role of reactive oxygen species/oxidants in causing apoptosis was clearly demonstrated in the case of the anticancer mitochondrial drug, elesclomol; this agent killed cancer cells by promoting oxidant production; simultaneous administration of NAC stopped preferential killing of cancer cells.
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