The consumption of O2 in the mitochondria is coupled to the synthesis of ATP from ADP and PO4 – i.e. in the absence of ADP, O2 consumption stops. O2 consumption could be restored in the absence of ADP by lipid soluble weak acids, which provided an alternative mechanism for protons to cross the inner mitochondrial membrane. The Role of Lipid-Soluble Weak Acids in Mitochondrial O2 Consumption and ATP Synthesis

Lipid-Soluble Acids’ Role in Mitochondrial O2 Consumption & ATP Synthesis

The subsequent synthesis and use of ATP is dependent on O2 intake in mitochondria. O2 intake ceases when ADP is absent (Kou and co-authors, 2018). A new study by Hu et al. (2016) has revealed a way to increase O2 consumption without ADP. This is through the use of weak acids, which are lipid-soluble. These weak acids were found to facilitate transport of protons through the inner membrane. This allows for ATP synthesis as well as O2 consumption. This study tested the hypothesis of the authors by measuring the oxygen intake of mitochondria isolated in the absence and presence of ADP. Their results showed that adding weak acids could increase O2 consumption by as much as 30% to 50%, which suggests that they are able to restore O2 in absence of ADP. The authors also found that weak acids did not have an effect on O2 intake when ADP was present. This suggests that weak acids are only effective in restoring O2 to those who lack ADP (Hu and al., 2016,). Cont…..

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