• NADH
  • ΔGf = Σ ΔGfp − ΔGfo C2H6O(Ethanol) + NAD+ →C2H4O(Acetaldehyde) + NADH + H+ Ethanol: −174.8 kJ/mol Acetaldehyde: −127.6 kJ/mol ΔGf1 = −127.6 + 174.8 = 47.2 kJ/mol(Endergonic) ΣΔGf = 47.2 kJ/mol (Endergonic, but this does not take into consideration the simultaneous reduction of NAD+. (wikipedia.org)
  • reactive oxygen
  • Boffetta and Hashibe list plausible mechanisms as including: a genotoxic effect of acetaldehyde increased oestrogen concentration a role as solvent for tobacco carcinogens production of reactive oxygen species and nitrogen species changes in folate metabolism Individuals who both smoke and drink are at a much higher risk of developing mouth, tracheal, and esophageal cancer. (wikipedia.org)
  • retinoic acid
  • induction of increased production of inhibitory guanine nucleotide regulatory proteins and components of extracellular signal-regulated kinase-mitogen-activated protein kinase signaling accumulation of iron and associated oxidative stress inactivation of the tumor suppressor gene BRCA1 and increased estrogen responsiveness (primarily in breast) impairment of retinoic acid metabolism. (wikipedia.org)
  • individuals
  • The increased exposure to acetaldehyde in individuals with the catalytically inactive form may also confer greater susceptibility to many types of cancer. (genecards.org)
  • activity
  • Every time stem cells divide, they become exposed to unavoidable errors associated with cell division (e.g., mutations arising during DNA replication and chromosomal alterations occurring during mitosis) and also become highly vulnerable to the genotoxic activity of DNA-damaging agents (e.g., acetaldehyde and tobacco carcinogens). (wikipedia.org)