Figure 9. (A) Schematic illustration of the possible mechanism of GTP cyclohydrolase I (GTPCH I) and tetrahydropterin (BH4) regulation of endothelial nitric oxide synthase (eNOS) expression and oxidative stress in experimental cryptorchidism. Experimental cryptorchid testes induced the increases in GTPCH I mRNA expression, BH4 levels, eNOS protein expression, NO concentration, and ONOO^– levels. (B) Oral administration of BH4 decreased GTPCH I mRNA and BH4 levels, with concomitant reduction of eNOS protein levels, ONOO^– levels, and NO concentration, resulting in reduced testicular damage1.