Figure 1.

Non-genomic to Genomic Effects of 2,4-Dinitrophenol (DNP). The early immediate effects of DNP lower the mitochondrial membrane potential, which abolishes overt reactive oxygen species (ROS) production and subsequently closes the uniporter involved in calcium influx [28,29,30]. This event is considered “non-genomic” since the target is a location, the mitochondrial matrix, vs. a protein, receptor or gene. However, this effect increases cyclic adenosine monophosphate (cAMP) (2nd messenger), likely through activation of adenylate cyclase. The production of cAMP transitions the non-genomic event into a genomic event and induction of expression of a host of genes, both up-regulated and down-regulated. In particular, the DNP → cAMP → cAMP response element binding (CREB) → Brain-derived neurotrophic factor (BDNF) cascade lends itself to the possibility of increased cognition [30,31,32]. Calcium graph was adapted from Liu, et al. 2015 [30].