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. Author manuscript; available in PMC: 2014 Jun 16.
Published in final edited form as: Expert Opin Ther Targets. 2013 Apr 22;17(7):839–855. doi: 10.1517/14728222.2013.791679

Figure 2. A schematic drawing illustrating the effects of EDCs on steroidogenesis in mammalian Leydig cells.

Figure 2

Following the binding of LH to G-protein coupled LH receptor, it stimulates adenylate cyclase (AC), leading to a surge in intracellular cyclic AMP (cAMP). Activated cAMP and ligand binding of peroxisome proliferator activated receptor gamma (PPARγ) stimulate the phosphorylation of protein kinase A (PKA), which in turn initiate gene transcription of StAR protein. StAR gene expression can be further up-regulated by thyroid hormones and Insulin-like growth factor-1 (IGF-1) stimulation. StAR protein in the outer mitochondrial membrane is responsible for the transportation of precursor cholesterol to the inner membrane where P450scc (cholesterol side-chain cleavage enzyme, labeled as P450sc) was found. Cholesterol is converted to pregnenolone where it goes to the smooth endoplasmic reticulum (ER) for further enzymatic conversion to testosterone and estrogen. Different EDCs impose adverse effects which ultimately lead to the disrupted biosynthesis of male sex hormone testosterone that perturbs spermatogenesis.