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ABS TRACT Ob jec ti ve: To in ves ti ga te the bi oc he mi cal ef fects of lep tin and lep tin plus L-NA ME on re ti nal nit rot yro si ne, ma lon di al dehy de, and su pe ro xi de dis mu ta se le vels in a mo del of hyper car bic oxy gen in du ced re ti no pathy in rats. Ma te ri al and Met hods: Forty new born rat pups we re di vi ded in to four gro ups con sis ting of lep tin, lep tin plus L-NA ME, hype ro xi a and sham gro ups. All gro ups, ex cept the sham gro up, we re ex po sed to ten mi nu tes of hyper car bi a fol lo wed by ten mi nu tes of hy pe ro xi a twi ce a day with an in ter val of 30 mi nu tes. This pro to col was per for med for three days and then pups we re sac ri fi ced. The re ti nas we re dis sec ted and re ti nal nit rot yro si ne, su pe ro xi de dis mu ta se and ma lon di al dehy de le vels we re me a su red. Re sults: The hig hest re ti nal nit rot yro si ne le vels we re me a su red in the lep tin gro up fol lo wed by the hype ro xi a gro up (p< 0.05). Lep tin plus L-NA ME and the sham gro up sho wed si mi lar re sults, in di ca ting an an ti o xi da ti ve ro le for L-NA ME (p< 0.05). Su pe ro xi de dis mu ta se le vels we re al so lo wer in the Lep tin plus L-NA ME gro up when com pa red to the hype ro xi a gro up (p< 0.05). Conc lu si on: This study sho wed that lep tin-in du ced re ti nal oxi da ti on may be pre ven ted by nit ric oxi de syntha se in hi bi tors. We sho wed the pro tec ti ve ro le of L-NA ME aga inst nit ric oxi de me di a ted pe roxy nit ri te to xi city. Furt her re se arch sho uld be car ri ed out to in ves ti ga te the ro le of nit rot yro si ne on oxy gen in du ced re ti no pathy.

The Effect of L-NAME Treatment on Leptin Associated Retinal Nitrosylation in Hypercarbic Oxygen Induced Retinopathy in Newborn Rats