Metabolic mechanisms of methanol/formaldehyde in isolated rat hepatocytes: Carbonyl-metabolizing enzymes versus oxidative stress

Is nonalcoholic fatty liver disease an endogenous alcoholic fatty liver disease? – A mechanistic hypothesis

“…These include obstructive sleep apnea-induced hypoxia [71,72], by-products of both carbohydrate [73][74][75][76][77] and lipid metabolism [78][79][80], and gut-derived bacterial toxins [81,82]. Furthermore, nonoxidative metabolites of ethanol [19,83,84], methanol/formaldehyde [27,85,86], and nitrosative stressors [87,88] may also contribute to NAFLD pathogenesis.…”

Activity of phosphatase-sensitive 5-aminolevulinic acid prodrugs in cancer cell lines

“…44 Formaldehyde disposal from cells include its reduction to methanol via the cytosolic alcohol dehydrogenase (ADH) or by the oxidation to formate catalyzed by ADH3 in the cytosol or by aldehyde dehydrogenase (ALDH) in the mitochondria. [45][46][47] It has already been reported that formaldehyde forming prodrugs can have enhanced cytotoxic effects that are cell type dependent, prodrug concentration and the formaldehyde concentration dependent. 48 The latter may apply on the results obtained by monitoring the PpIX production in different cancer cell types ( Figure 3, 4, S1 and S2).…”

FructationIn Vivo: Detrimental and Protective Effects of Fructose

“…In contrast to glucose, fructose inhibited apoptosis induced by reoxygenation in rat hepatocytes by decreasing the level of ROS [17]. Fructose has also been found to defend rat hepatocytes against exogenous oxidative stress [18, 20]. It has been demonstrated that fructose and its phosphorylated derivatives such as fructose-1,6-bisphosphate had significantly higher antioxidant capacities against ROS than other carbohydrates [22].…”