Acclimation of plants to O 2 deprivation depends on their ability to mitigate detrimental effects related to energy crisis and cytosolic acidosis. Accordingly , lactic and ethanol fermentative pathways are activated under low oxygen stress in order to regenerate NAD + to maintain a high glycolysis rate that becomes the major route for ATP production. Paradoxically lactic acid worsens cytosolic acidosis and ethanol fermentation drains carbon for the production of a metabolically useless dead-end product. Nitrogen metabolism is profoundly affected by O 2 deprivation. Interestingly hypoxic N metabolism not only contributes to tolerate O 2 deprivation but also mitigates negative effects of lactic and ethanol fermentation. The most salient event is the concerted modulation of alanine and glutamate pathways that allow for the substitution of ATP-dependent enzymes glutamine synthetase (GS) and asparagine synthetase (AS) by alanine aminotransferase (AlaAT) and glutamate oxoglutarate aminotransferase (NADH-GOGAT) as essential enzymes of N assimilation. This adaptation saves ATP, regenerates NAD + , and saves carbon in the form of alanine, a C/N storage form readily remobilized upon recovery. As for acidosis amelioration, nitrogen metabolism participates in the cellular pH-stat through GABA and putrescine pathways. Alanine accumulation contributes indirectly to pH homeostasis by using pyruvate competitively with lactate dehydrogenase.