Autophagy compensates Against BPA Induced Cytotoxicity in Neural Cells

Autophagy induces loss of ROS production and antioxidant gene expression as a protective response against BPA, BPA exposure causes intracellular damage and causes intracellular ROS production. PMA: 22996013. BPA decreases the expression of antioxidant genes and causes various types of toxicity PMID: 22888396. Autophagy functions as an intracellular protection mechanism. PMID: 12865942 Here we explain exposure to BPA as a cellular self-compensating response. Here, we observed that the effect of autophagy again leads to BPA-induced oxidative damage.

Figure 4.3 Mechanism by which F 2 induces breast cancer cell death. Ginsenoside F2 causes DNA damage, which causes activation of p53 and downstream proteins, thereby inducing intrinsic apoptosis. Activation of mitochondrial apoptosis is accompanied by induction of defensive autophagy. CQ increased F2 induced CSC cytotoxicity, but PFT prevented apoptosis and partially inhibited autophagy. This suggests that p53 is not the only pathway mediating F2-induced autophagy. Several cases are known in which lysosomal membrane permeabilization (LMP) and subsequent release of cytotoxic hydrolase into the cytoplasm are involved in endogenous apoptosis (Boya and Kroemer, 2009; Boya et al., 2003; Kroemer And Jaattela, 2005). LMP can also promote the performance of necrotic cell death. Excess ROS rapidly outweighs the cell's antioxidant defense capacity, which can attack polyunsaturated fatty acids in the cell membrane and produce toxic aldehydes (eg 4-hydroxynonenal).

The correlation between autophagy and apoptosis is a new topic, especially in the field of cancer biology. On the other hand, autophagy induces cell death by degrading essential components, while on the other hand promotes cancer cell survival under harmful metabolic conditions. Various stimuli that may induce apoptosis may also cause autophagy. Here, autophagy can precede apoptosis and can be caused by a lower degree of stress. When apoptosis is suppressed, it leads to deterioration of autophagy. Therefore, autophagy can be thought of as a strategy for cells to cope with stress, but autophagy is inactivated when apoptosis begins. It has been noted that mitochondria are a switch between apoptosis and autophagy. If autophagy is blocked and damaged mitochondria are not excluded, they suffer a loss of transmembrane potential (ΔΨm) that can lead to apoptosis.