Objective: To investigate the effect of carbon disulfide (CS2) on inducible nitric oxide synthase (iNOS) and apoptosis in in the retina of rats.
Methods: Twenty-four male SD rats were randomly divided into 3 groups the control group, the group receiving high-dose CS2 and the group receiving low-dose CS2. After treatment, retina were harvested and made into slice. The thickness of inner retina including outer plexiform layer, inner nuclear layer, ganglion cell layer, optic nerve fiber and inner limiting membrane was measured. Expression of iNOS in retina was measured by NADPH-NDP histochemical assay. Apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL).
Results: (1) The thickness of inner retina decreased in groups receiving CS2. There was significant difference between control group and groups receiving CS2 (P < 0.05). There was also significant difference between group receiving high-dose CS2 and group receiving low-dose CS2 (P < 0.05). (2) The expression of iNOS increased in groups receiving CS2. There was significant difference between control group and groups receiving CS2 (P < 0.05 or P < 0.01). There was also significant difference between the group receiving high-dose CS2 and the group receiving low-dose CS2 (P < 0.05). (3) Apoptosis was observed in groups receiving CS2. There were significant differences in apoptosis index between the control group and groups receiving CS2 (P < 0.05 or P < 0.01). There was also significant difference between the group receiving high-dose CS2 and the group receiving low-dose CS2 (P < 0.05).
Conclusions: CS2 can evoke the expression of iNOS, and the nitric oxide thus produced can be one of the causes of retina destruction. And apoptosis is also one of the causes of retina destruction.