The present study aimed to explore the role of d-limonene in the management of diabetic neuropathy. Adult Wistar rats (either sex, 200-250 g) were divided into 6 groups (n=6). Diabetes was induced in overnight fasted rats by a single intraperitoneal injection of streptozotocin at a dose of 50 mg/kg body weight freshly dissolved in 0.1 mol/L citrate buffer, pH 4.4. D-limonene was administered in 2 doses (100 and 200 mg/kg; p.o.) to separate groups of rats for 35 successive days daily. Gabapentin (100 mg/kg; i.p) served as standard drug. The neuropathic activity was evaluated in streptozotocin induced diabetic neuropathicrats using Cold andhot water immersion test and tail flick test. After wards, the animals were sacrificed; sciatic nerve is isolated, homogenized and centrifuged for TBARS, GSH, nitrite, catalase and protein estimations. STZ induced diabetic neuropathy caused the decrease in body weight, decrease in tail-flick latency time in radiant heat apparatus, decrease tail-withdrawal latency in tail-immersion (warm water) test, decrease allodynic response in tail-immersion (cold water) test. Furthermore STZ induced diabetic neuropathic rats expressed higher sciatic nerve TBARS and nitrite levels and lower sciatic nerve GSH and catalase levels. D-limonene significantly attenuated (p<0.05) the behavioral and biochemical alterations produced by STZ induced diabetic neuropathy in rats. Catalase, GSH and total protein levels were restored (p< 0.05) in the d-limonene treated animals. D-limonene treated rats showed a significant (p< 0.05) decrease in nitrite and TBARS level. In conclusion, d-limonene may prove to be useful remedy for the management of diabetic neuropathy owing to its possible antioxidant properties.