Sodium azide (NaN 3 ), a well-known inhibitor of mitochondrial respiration, stimulated bud-dormancy release in grapevines similar to hydrogen cyanamide (HC), while HC, a well-known dormancy release agent, inhibited the O 2 uptake in isolated grape bud mitochondria similarly to NaN 3 . Additionally, both chemicals induced transcript expression of the antioxidative enzyme glutathione reductase and glucose-6-phosphate-dehydrogenase (G6PD), therefore upregulated the ascorbate-glutathione cycle (AGC) and the pentose phosphate pathway, respectively. As a result of AGC activation, the ratio of reduced to oxidized glutathione (GSH/GSSG) increased. Both stimuli also upregulated the transcription of 1,3-b-D-glucanase, a key enzyme in dormancy release. Together, these data support mechanistic connection between impaired Mit function and dormancy release, and suggests that as a consequence of O 2 deprivation, increases in glycolysis and in ethanolic fermentation could be responsible for activation of downstream stages in the dormancy release mechanisms.