Abstract

The impact of the individual and combined action of dehydration and low temperature on the respiratory activity of mitochondria isolated from epicotyls of pea (Pisum sativum L.) seedlings was investigated. These organelles were isolated immediately after the treatments and after two and three days of recovery. After the treatments, the capacity of the energy-producing cytochrome pathway (CP) of mitochondrial oxidation decreased, while the capacity of the non-phosphorylating alternative respiratory pathway (AP) catalyzed by a CN-resistant oxidase was elevated. After returning the seedlings to normal growing conditions, a gradual recovery of the respiratory activity of mitochondria was observed due to the inactivation of the AP and an elevation of the activity of the CP. The dehydration was a strong stress factor and led to a more significant disturbance of mitochondrial functioning than low temperature, and the complete recovery of the respiratory activity was observed only after the combined action of these stress factors. The post-stress reactivation of malate rather than succinate oxidation required a longer maintenance of seedlings under the control conditions.

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