In the present study, the influence of cold restraint stress (CRS)-induced gastric
damage in diabetic rats, in relation to the antioxidative system was investigated. Male
albino rats were used in the study, they were divided into 5 groups: i): non stressed
group, ii): control CRS group, iii) diabetic CRS group (the rats of this group were
injected with streptozotocin (STZ) 70 mg/kg i.p. and used 4 weeks after induction of
diabetes with blood glucose levels of >350 mg/dl), iv): STZ L-carnitine pretreatment
group (STZ-induced diabetic rat of this group were given L-carnitine 500 mg/kg 30
min before CRS) and v): STZ-vitamine E pretreatment group (STZ-induced diabetic
rat of this group were given vitamin E 60 mg/kg body wt three weeks before CRS).
The last four groups were exposed to CRS, at the end of each experiment, gastric
damage was observed macroscopically. CRS induced gastric lesion, that was
markedly exacerbated in STZ diabetic rats, but this aggravation was significantly
suppressed by pretreatment with either L-carnitine or tocopherol (vitamin E)
pretreatments. Diabetic rat stomachs showed significantly less glutathione peroxidase
(GPX) activity as well as reduced glutathione (GSH) content than normal rat
stomachs. In addition, the deleterious influence of diabetes on the gastric ulcerogenic
response to CRS was significantly mitigated by decreasing lipid peroxidation by
pretreatment with either L-carnitine or vitamin E. These results suggest that the
gastric mucosa of diabetic rats is more vulnerable to cold restraint–induced injury,
and the mechanism may be partly accounted for by impairment of the antioxidative
system associated with a reduced GPX activity and GSH content. Based on these
data, the beneficial effects of L-carnitine and vitamin E on CRS-induced mucosal
injury especially in diabetics may be attributed to their antioxidative effects.