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Characterization of internal validity threats to phase III clinical trials for chemotherapy-induced peripheral neuropathy management: a systematic review

Finally, for therapy effect of BPC 157 on paracetamol brain injury in rats that received pentadecapeptide BPC 157 later in an advanced paracetamol toxicity stage, we should consider that at the time point of 3 hours following paracetamol, as previously mentioned, after therapy these rats had initially exhibited generalized convulsions and had significant brain damage

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Ferroptosis is classified under regulated types of cell death relying on dedicated molecular machinery, and as such, can be induced/prevented by different pharmacological/genetic manipulations

[300-303] But it is a type of chelator that does not redistribute to other tissues, which is a big risk in many chelation therapies.[304-308] Natural compounds such as N-acetyl L-cysteine, alpha lipoic acid and glutathione all contribute to chelation and excretion of metals in the human body with much less risk of displacement into other tissues, such as the brain, than synthetic chelating agents.[309,310] These compounds also serve as antioxidants in the tissue to protect the tissue from damage caused by interaction with heavy metals.[311-313] Oxidative stress may be considered as one of the prime contributing mechanisms in metal toxicity and thus provide a strong rationale for including antioxidants during chelation therapy.[314] Antioxidant supplementation with chelating agents has been found beneficial in increasing metal mobilization and providing improved recovery from problems associated with chelation therapy [315-317]