Abstract
There is evidence that L‐cysteine, the substrate for biosynthesis of hydrogen sulfide (H2S) can regulate potassium (K+)‐evoked glutamate release from bovine isolated retina. In the present study, we compared the pharmacological effects of the precursor for L‐cysteine, N‐acetyl cysteine (NAC) to that of L‐cysteine on K+‐evoked [3H]D‐aspartate release, and on glutamate‐induced neurotoxicity in bovine isolated retina. Isolated neural retina were incubated in oxygenated Krebs solution containing 200 nM of [3H]D‐aspartate and then prepared for studies of neurotransmitter release. The 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay was used to assess retinal neuron survival. Both L‐cysteine (0.1 µM to 10 µM) and NAC (10 µM to 1 mM) elicited a concentration‐dependent inhibition of K+‐induced [3H]D‐aspartate release. At an equimolar concentration of 10 µM, both L‐cysteine and NAC reduced [3H]D‐aspartate release by 54.3% (p < 0.001) and 8.3%, respectively. Interestingly, L‐cysteine (1 mM) and NAC (1 µM) attenuated glutamate (12 mM)‐induced neuron degeneration by 31.1% (p<0.05) and 18.4%, respectively. L‐cysteine was more potent in attenuating neurotransmitter release while NAC was more effective in preventing glutamate‐induced toxicity suggesting that these compounds mediate their pharmacological actions via different mechanisms.