The influence of the metabolic status of mitochondria upon their radiation response was studied. It turned out that the reduction of pyridine nucleotides by addition of beta-hydroxybutyrate (BOH) and the decrease through respiration were distinctly impaired in mitochondria with a substrate deficit by an irradiation with 2.7 krd already. The evolution of the lesion depends on the incubation conditions following irradiation, a presence of BOH having protective effects. The general redox level seems to be essential for radiation response of mitochondria. An exit of NAD from mitochondria has proved to be the main cause for inhibition of the respiratory BOH-consumption.
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