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 can be stopped if there is no ADP (Kou et. al. 2018, 2018). A recent study found that lipid-soluble weak acid (Hu and co., 2016) can be used to replenish O2 intake in the absence ADP. The weak acids could facilitate protons transport across the inner membrane. Thus, ATP synthesis can be enabled and O2 consumption is possible. The authors tested this hypothesis by monitoring the oxygen consumption in isolated mitochondria when ADP was present or absent (Hu and co-authors, 2016). The addition of weak acids to O2 increased O2 intake by between 30-50% and 60%, indicating that it is an efficient mechanism to restore O2 in absence of ADP (Hu, et al. 2016). 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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