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indicates that PAC, in the absence of adequate, physiological levels of GSH, may give rise to genotoxic quinone imine metabolites ( The production of quinone imine metabolite is the primary responsible for PAC liver and kidney toxicity

Remarkably, the more pronounced actions of this combination over other studied treatments may be ascribed to the abilities of the tested agents to boost antioxidant defense, hamper neuroinflammation, suppress ER stress, hinder neuronal apoptosis, enhance neurotrophic activities and promote autophagic machineries, via their modulatory actions on HMGB1/RAGE/JAK-2/STAT-3, PERK/CHOP, PI3K/AKT/CREB/BDNF and AMPK/SIRT-1 hubs

Action of GH on skeletal muscle function: Molecular and metabolic mechanisms

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