SynopsisAll plants are able to survive anoxic periods, but the degree of tolerance shows large variation. The main injuries related to anoxia are eventually due to changes in energy metabolism. Low energy charge values indicate a cessation of many ATP consuming processes. Sugar starvation, lactic acid fermentation and proton release from leaky vacuoles are responsible for cell death. Long-term anoxia tolerance is dependent on storage products in the vicinity of sinks, on an adequate control of glycolysis, synthesis of essential proteins, and stability of membranes and organelles. However, no fundamental differences between the metabolic pathways of tolerant and non-tolerant tissues are known. It is rather a question of minor changes and the regulation of anaerobic metabolism.Re-exposure of anoxic tissues to air may even be more detrimental than anoxia itself. These injuries are mainly due to enhanced radical generation. Lipid peroxidation processes lead to membrane damage, disintegration, and leakage of solutes. Under natural conditions plants are equipped with radicaldetoxifying systems (SOD, peroxidases and antioxidants). Natural detoxifying systems can be reduced in non-adapted plants under anoxia and they become more sensitive to post-anoxic damage. In addition, the rapid conversion of ethanol to extremely toxic acetaldehyde seems to be a cause of tissue injury and death.

Potato tubers kept under hypoxia (1%) showed improved viability in comparison to anoxia, which was associated with the maintenance of intermediate adenvlate ener,w charge values (A.E.C. = 0.6) and stable adenylate pools at 50% of the initial levels. Re-admission of oxygen to the tuber resulted in an almost full recovery of adenylate energy charge and total adenylates after up to 3 days of hypoxic pretreatment. Tubers exhibited a mixed fermentation. The high lactate. ethanol and acetaldehyde levels proved to be non toxic. Ethanol was degraded to acetaldehyde during re-aeration. Posthypoxic lipid peroxidation was indicated by malondialdehvde and ethane formation. Both products occurred with a temporary delay and in lower amounts compared to post-anoxia. Ethylene release was also considerably smaller. Severe hypoxia and posthypoxia postponed tissue death compared to anoxia. Survival was correlated with an improved energy supply which stabilized membranes.