Background Cataracts is considered be formed because of an abnormal glucose metabohc pathway oroxidative stress.We explored the damaging role of ONOO~- and antagonism of cholecystokinin octapeptide-8(CCK-8)in diabetic cataractal rat lenses.Methods A diabetic cataractal animal model was established by peritoneal injection of streptozotocine(STZ).Thirty-six normal SD rats were taken as control group;seventy-two were given STZ(45 mg/kg)and then dividedinto STZ group and CCK-8 group(peritoneal injection CCK-8).STZ induced diabetic rats were treated withCCK-8 for 60 days.Lenses were examined with slit lamp at 20,40 and 60 days.Immunofluorescent stainingand Western blot analysis were used for determining nitrotyrosine(NT,a marker for ONOO~-).RT-PCR andgene array analysis were used for determining the expression of inducible nitric oxide synthetase mRNA(iNOSmRNA)in lens epithelium(LEC).Results STZ group rats developed lens opacity by 20 days that reached a high level by 60 days after STZinjection.CCK-8 group rats delayed the cataract formation.There was no distinct expression of NT and iNOSmRNA in control group.In STZ group,there were distinct expression of NT and upregulation of iNOS mRNA;however,CCK-8 group showed weak expression of NT and downregulation of iNOS mRNA.Conclusions NT,which may be a new form of oxidative stress,was expressed in diabetic rat LEC althoughCCK-8 could reverse NT damage in LEC.The results suggested that CCK-8 might be a useful therapeutic agentagainst diabetic cataract.The antagonizing mechanism of CCK-8 may be related to direct antagonism of ONOO~-as well as its inhibition of the expression of iNOS mRNA for production of NO and therefore decrease in theformation of ONOO~-. Background Cataracts was considered as formed by of an abnormal glucose metabohc pathway or oxidative stress. We explored the damaging role of ONOO ~ - and antagonism of cholecystokinin octapeptide-8 (CCK-8) in diabetic cataractal rat lenses. Methods A diabetic cataractal animal model was established by peritoneal injection of streptozotocine (STZ). Thirty-six normal SD rats were taken as control group; seventy-two were given STZ (45 mg / kg) and then dividedinto STZ group and CCK-8 group ). STZ induced diabetic rats were treated with CCK-8 for 60 days. Lenses were examined with slit lamp at 20, 40 and 60 days. Immunofluorescent staining and Western blot analysis were used for determining nitrotyrosine (NT, a marker for ONOO ~ -). RT-PCR and gene array analysis were used to determine the expression of inducible nitric oxide synthetase mRNA (iNOS mRNA) in lens epithelium (LEC). Results STZ group rats developed lens opacity by 20 days that reached a high level by 60 days after STZinjec tion. CCK-8 group rats delayed the cataract formation. There was no distinct expression of NT and iNOS mRNA in control group. STZ group, there were distinct expression of NT and upregulation of iNOS mRNA; however, CCK-8 group showed weak expression of NT and downregulation of iNOS mRNA. Conclusions NT, which may be a new form of oxidative stress, was expressed in diabetic rat LEC although CCK-8 could reverse NT damage in LEC. These results suggested that CCK-8 might be a useful therapeutic agent for cancer diabetic cataract. The antagonizing mechanism of CCK-8 may be related to direct antagonism of ONOO ~ -as well as its inhibition of the expression of iNOS mRNA for production of NO and therefore decrease in theformation of ONOO ~ -.