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Inhibition of rat heart mitochondrial electron transport in vitro: implications for the cardiotoxic action of allylamine or its primary metabolite, acrolein.
Biagini RE; Toraason MA; Lynch DW; Winston GW
Toxicology 1990 May; 62(1):95-106
A examination was conducted of the effects of allylamine (107119) and acrolein (107028) on electron transport and oxidative phosphorylation in mitochondria isolated from hearts of male Sprague- Dawley-rats. Both acrolein and allylamine inhibited State-III, State-IV, and uncoupler stimulated respiration in a concentration dependent fashion when added to mitochondria respiring on glutamate, malate, and malonate (GMM) as substrate. While the concentration dependent inhibitory effect was statistically greater for acrolein than allylamine for State-III and uncoupler stimulated oxygen uptake, the concentrations necessary to produce these effects were in the millimolar range for both compounds. Allylamine and acrolein also displayed concentration dependent effects on respiratory enzyme activities in mitochondria actively respiring on succinate as substrate. State-III, State-IV, and uncoupler stimulated oxygen uptake were significantly inhibited by increasing concentration of allylamine or acrolein. In contrast to the results obtained with GMM, with succinate as substrate no significant differences between allylamine and acrolein in concentration effect slopes were noted for State-III, State-IV and uncoupler stimulated activities, indicating site selectively between the two compounds. Respiratory control ratios were significantly decreased by allylamine and acrolein with GMM as substrate. When succinate was used as substrate, the respiratory control ratio was significantly reduced only by acrolein, again suggesting the site selective nature of this compound.
NIOSH-Author; Cell-function; Cell-damage; ardiovascular-system-disorders; Amines; Herbicides; In-vitro-study; Oxidative-phosphorylation
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