The adverse alterations in mitochondrial functions can affect neuronal function negatively, as they play a crucial role in neuronal plasticity and death. Direct measurements of mitochondrial activity, including membrane potential and ATP production, are not easily achieved in post-mortem brain and liver samples because most organ functions cease to work after death; in fact, with increasing post-mortem intervals (PMI), the brain and liver tissues deteriorate rapidly. Standard procedures of mitochondria isolation, protein determination expressed as BSA equivalent, and spectrophotometric assessment of pore opening at 540 nm were employed.
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