EFFECTS OF GLUCOSE STARVATION ON THE OXIDATION OF FATTY-ACIDS BY MAIZE ROOT-TIP MITOCHONDRIA AND PEROXISOMES - EVIDENCE FOR MITOCHONDRIAL FATTY-ACID BETA-OXIDATION AND ACYL-COA DEHYDROGENASE-ACTIVITY IN A HIGHER-PLANT

Fatty acid beta-oxidatiOn was studied in organellar fractions from mai ze root tips by h.p.l.c. and radiometric analysis of the products of i ncubations with [1-C-14]octanoate and [1-C-14]palmitate. In crude orga nellar fractions containing both mitochondria and peroxisomes, octanoa te and palmitate beta-oxidation, as determined by the production of ac etyl-CoA, was functional and, for palmitate, was activated 4-12-fold a fter subjecting the root tips to 48 h of glucose starvation. The sensi tivity to a 'cocktail' of respiratory-chain inhibitors containing cyan ide, azide and salicyl-hydroxamate depended on the conditions of incub ation, with no inhibition in a medium facilitating peroxisomal beta-ox idation and a significant inhibition in a medium potentially facilitat ing mitochondrial beta-oxidation. Indeed, preparations of highly purif ied mitochondria from glucose-starved root tips were able to oxidize o ctanoate and palmitate to give organic acids of the tricarboxylic acid cycle. This activity was inhibited 5-10-fold by the above cocktail of respiratory-chain inhibitors, with no parallel accumulation of acetyl -CoA, thus showing that the inhibition affected beta-oxidation rather than the pathway from acetyl-CoA to the organic acids. This provides t he first evidence that the complete beta-oxidation pathway from fatty acids to citrate was functional in mitochondria from a higher plant. M oreover, an acyl-CoA dehydrogenase activity was shown to be present in the purified mitochondria. In contrast with the peroxisomal activity, mitochondrial beta-oxidation showed the same efficiency with octanoat e and palmitate and was strictly dependent on glucose starvation.