Short term feeding of hexadienal to postnatal rats: effects on stomach aldehyde dehydrogenase

Since a number of food and food products contain 2,4-hexadienal (HX), an unsaturated aldehyde, human exposure to HX is likely. Long term HX feeding to rodents induces forestomach cancers. Aldehyde dehydrogenases (ALDH) are key enzymes in the stomach for the metabolism of aldehydes. We examined the effect of short term feeding of HX on ALDH activity using HX as the substrate (HXDH) in different tissues of the GI tract. Feeding HX at a dose of 200 mg/kg body weight/day to post-suckling rats for 5 days elevated HXDH activity in the forestomach and esophagus but not in the glandular stomach, liver, small intestine or kidney. The induction of HXDH by HX was evident at 12.5 mg/kg dose and showed a dose-dependence up to 200 mg/kg. Increase in HXDH was time dependent but detectable after the first feeding (1 day). A similar dose (200 mg/kg) of acetylaldehyde or ethanol had no effect on HXDH activity. The increase in HXDH level in the forestomach and esophagus was transient. HXDH activity returned to normal 4 days after withdrawal of HX. Zymograms of gastric HXDH isozyme patterns in control and HX-fed counterparts were similar but showed selective increase in two particular forms in the forestomach. It is possible that these isoforms metabolize HX differently resulting in an accumulation of potential carcinogenic metabolites within the forestomach.