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Chemotherapeutic ROS and calcium overload depolarise the mitochondrial inner membrane, exhaust ATP reserves and foster release of pro-apoptotic factors [87,88,89]

While intermediate metabolites associated with TCA cycle (Tricarboxylic Acid Cycle) such as fumarate, succinate, and malate were not significantly different between the groups, we suggest a decrease in mitochondrial activity may result in lower ATP generation as reported in other inflammatory conditions (65, 66)