From reading posts in the forum here I see that some studies have potentially linked NAC suplementation to increased incidents of cancer, where the route of action is thought to be an improved mechanism of protection for cancer cells that may already be present.
Most of these posts are late 2022, so I was wondering if there had been any new research or evidence that has come to light in the intervening year to clarify whether this may or may not be correct?
The clearest and most nuanced I’ve found so far is this:
At low levels, superoxide/H2O2 induce cell proliferation and promote tumorigenesis and progression, and at higher levels they are cytotoxic to cancer cells and inhibit metastasis. Thus, inhibiting ROS could mitigate tumorigenesis and progression while stimulating metastasis. Antioxidants that directly or indirectly remove ROS affect tumorigenesis, progression, and metastasis of tumor cells differently. NAC was shown to exert paradoxical effects in a mouse lung cancer model [17,18]. NAC treatment enhanced metastasis of lung cancer [16,17]. This could be due to decreased oxidative stress in metastatic tumors, causing them to proliferate and grow in distant sites . Pretreatment of melanoma cells with NAC prior to intravenous injection in mice enhanced tumor formation by tenfold . The findings from the mouse melanoma progression model predict that the use of dietary antioxidants or antioxidant therapy might protect against the deleterious effects of oxidants in metastatic melanoma cells, and that the antioxidant therapy is a contraindication for melanoma .
NAC can inhibit the anti cancer effects of piperlongumine. I have seen a couple of research papers that show NAC could be detrimental to cancer. But the GLY/NAC study on mice gives a completely different picture. Mice are little cancer factories. Most mice die fron cancers, and yet their lifespan is increased in a profound way when they are given GLY/NAC.
Honestly, I don’t know how to interpret this.
“Piperlongumine selectively kills glioblastoma multiforme cells via reactive oxygen species accumulation dependent JNK and p38 activation. Antioxidant N-acetyl-l-cysteine (NAC) completely reversed PL-induced ROS accumulation and prevented cell death in LN229 and U87 cells. In LN229 and U87 cells, PL-treatment activated JNK and p38 but not Erk and Akt, in a dosage-dependent manner.”