Abstract
The metabolism of malonaldehyde (MA) was investigated in vivo using male Wistar rats and in vitro using rat liver mitochondria. Twelve hr after intubation with [1,3-14C] MA, 60–70%, 5–15% and 9–17% of administered radioactivity was recovered in expired CO2, feces and urine, respectively. In rats intubated with [1,2-14C] acetate, the corresponding values were 68–82%, 1–2% and 2–3%.14CO2 evolution was initially slower after14C-MA administration than after14C-acetate administration and more radioactivity was excreted in the feces and urine. In vitro experiments using [1,3-14C] MA showed that MA is metabolized primarily in the mitochondria via reactions involving O2 utilization and14CO2 production. The apparent Km and Vmax were 0.5 mM and 9.3 nmol/min/mg protein for O2 uptake, respectively, and 2.0 mM and 2.4 nmol/min/mg protein for14CO2 production. Addition of malonic acid to mitochondrial incubates at concentrations inhibitory to succinate dehydrogenase did not affect MA-induced O2 uptake but enhanced14CO2 production from14C-MA.14C-Acetate appeared to be the major accumulating metabolite in rat liver mitochondrial preparations following a 120-min incubation with14C-MA. A probable biochemical route for MA metabolism involves oxidation of MA by mitochondrial aldehyde dehydrogenase followed by decarboxylation to produce CO2 and acetate.
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Siu, G.M., Draper, H.H. Metabolism of malonaldehyde in vivo and in vitro. Lipids 17, 349–355 (1982). https://doi.org/10.1007/BF02535193
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DOI: https://doi.org/10.1007/BF02535193