: Apoptosis is a programmed cell death that occurs due to the production of several catabolic enzymes. During this process, several morphological and biochemical changes occur in mitochondria, the main organelle in the cell that participates in apoptosis and controls apoptotic pathways. During apoptosis, cytochrome c is released from mitochondria, and different proteins activate caspase cascades that carry out the cell towards the death process. Apoptosis mainly occurs due to p53 protein that allows the abnormal cells to proliferate. Bcl-2 and Bcl-xl are two anti-apoptotic members of the protein family that prevents apoptosis. The membrane potential of mitochondria decreases by the opening of the permeability transition pore (PTP). These PTP are formed by the binding of Bax with adenine nucleotide translocator (ANT) and cause depolarization in the membrane. The depolarization releases apoptogenic factors (cytochrome c) that result in the loss of oxidative phosphorylation. Knockdown in lactate dehydrogenase (LDH) is the cause of the decrease in mitochondrial membrane potential elevating the levels of reactive oxygen species (ROS) and Bax. Consequently, causing an increase in the release of cytochrome c that ultimately leads to apoptosis. In this review, we have summarized the combined effect of mitochondrial membrane potential and LDH enzyme that triggers apoptosis in cells and their role in the mechanism of apoptosis.

: Epigenetic regulations play a crucial role in the expression of various genes that are important in the normal cell function. Any alteration in these epigenetic mechanisms can lead to the modification of histone and DNA, resulting in the silencing or enhanced expression of some genes causing various diseases. Acetylation, methylation, ribosylation, or phosphorylation of histone proteins modifies its interaction with the DNA, consequently changing the ratio of heterochromatin and euchromatin. Terminal lysine residues of histone proteins serve as potential targets of such epigenetic modifications. The current review focuses on the histone modifications, and their contributing factors; the role of these modifications on metabolism leads to cancer, and methylation of histone in cancer affects the DNA repair mechanisms.