Abstract
Previous work has shown a reduction in cephaloridine nephrotoxicity in a diabetic rat model. The following studies examinedin vitrocephaloridine toxicity in renal slices from normoglycemic and diabetic Fischer 344 rats. Diabetes was induced by acute intraperitoneal injection of 35 mg/kg streptozotocin. Renal cortical slices were isolated from normoglycemic and diabetic animals. Tissues were exposed to 0–5 mmcephaloridine for 15–120 min. Pyruvate-directed gluconeogenesis was diminished in all groups exposed to 2–5 mmcephaloridine for 60–120 min. Leakage of lactate dehydrogenase (LDH) was apparent only in the normoglycemic group in the presence of 4–5 mmcephaloridine for 120 min. LDH leakagewas notincreased at any cephaloridine concentration in the diabetic tissue. Total glutathione levels were compared in renal cortical slices exposed to cephaloridine for 30–120 min. Baseline values for glutathione were comparable between normoglycemic and diabetic tissue suggesting that the mechanism for reduced toxicity was not due to higher glutathione levels in diabetic tissue. Total glutathione levels were diminished more rapidly in normoglycemic than diabetic tissue by incubation with 5 mmcephaloridine. Comparison of cephaloridine accumulation indicated that diabetic tissue accumulated less cephaloridine than the normoglycemic group when tissues were incubated with 0–2 mmcephaloridine. However, renal slice accumulation was similar between normoglycemic and diabetic groups followingin vitroincubation with 4–5 mmcephaloridine. These results suggest that the mechanism for reducedin vitrocephaloridine toxicity in diabetic tissue cannot be limited to differences in accumulation and must include an unidentified cellular component.
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