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Abstract
This study investigated the effect of heme oxygenase (HO) inhibition on visual evoked potentials (VEPs). HO catalyzes the oxidative degradation of heme. Products of HO reaction are biliverdin, ferrous iron, and carbon monoxide (CO). CO is a signal molecule and is an endogenous modulator in the soluble guanylate cyclase/cyclic guanosine monophosphate signaling pathway. Rats were treated with HO inhibitors tin protoporphyrin IX (SnPP IX) or zinc protoporphyrin IX (ZnPP IX) or HO inducer sodium arsenite (Na-arsenite). Soluble guanylate cyclase is inhibited by 1H-[1,2,3]oxydiazolo[4,3-a]quinoxalin-1-one (ODQ) and induced by 3-(5′-hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1). VEPs were recorded under mild ether anesthesia with the help of stainless steel subdermal electrodes and a photic stimulator. SnPP IX, ODQ or SnPP IX + YC-1 injections significantly prolonged latencies of P3; however, Na-arsenite shortened latency of P3. It has been shown that HO affects VEPs.