The primary objective of this investigation was to assess the neuroprotective efficacy of spice active principles namely Eugenol (Eug) and isoeugenol (IE) in an acrylamide (ACR) neuropathy model in rats. In the present study, ACR administration (50 mg/kg bw, i.p. 3 times/week) for 5 weeks to growing rats caused typical symptoms of neuropathy. We found that treatment of ACR rats with spice active principles (10 mg/kg bw, for 5 weeks) caused marked improvement in gait score and responses in a battery of behavioral tests. Terminally, both spice active principles markedly attenuated ACR-induced markers of oxidative stress viz., reactive oxygen species (ROS), malondialdehyde (MDA) and nitric oxide (NO) in sciatic nerve (SN) as well as brain regions (cortex Ct, cerebellum Cb). Treatment with Eug restored the reduced glutathione levels in SN and brain regions. Interestingly, both spice active principles effectively diminished ACR-induced elevation in cytosolic calcium levels and acetylcholinesterase activity in SN and Ct. Further, the diminished activity of ATPase among ACR rats was enhanced in SN and restored in brain regions. Furthermore, Eug treatment significantly offset ACR-induced depletion in dopamine levels in brain regions. Collectively our findings suggest the propensity of these spice active principles to attenuate ACR-induced neuropathy. Further studies are necessary to understand the precise molecular mechanism/s by which these spice active principles attenuate neuropathy. Nevertheless, our data clearly demonstrate the beneficial effects of spice active principles in ACR-induced neuropathy in rats and suggest their possible therapeutic usage as an adjuvant in the management of other forms of neuropathy in humans.

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Involvement of oxidative stress, inflammatory response, and mitochondrial dysfunction in the development of diabetic neuropathy (DN) is well appreciated. The present study examines the potential of geraniol (GE), a well-known phytoconstituent commonly found in lemon, spices, rose oil, etc., to attenuate DN-associated oxidative/nitrosative stress by employing a streptozotocin (STZ) diabetic rat model. STZ-induced diabetic rats provided with oral supplements of GE (100 mg/kg bw/day, 8 weeks) exhibited significant improvement in tail-flick latency (sensory function) and the narrow beam test (motor function). Terminally, elevated levels of oxidative markers (reactive oxygen species, malondialdehyde, hydroperoxides) in cytosol of the sciatic nerve (SN) and in selected regions of the brain of diabetic rats were markedly reduced by GE supplements. Furthermore, GE significantly diminished the levels of protein carbonyls (a measure of protein oxidation) and nitrites in diabetic rats. In addition, in mitochondria, GE supplements restored the activities of enzymes, such as complexes I-III, succinate dehydrogenase, and citrate synthase, in brain regions of diabetic rats, with a concomitant reduction in the levels of oxidative markers. GE significantly lowered the enhanced cytosolic calcium levels and acetylcholinesterase activity in the SN and the brain regions of diabetic rats. Depleted dopamine levels evident in the SN and the cortex/striatum among diabetic rats were restored by GE. From our data, we hypothesize that GE may be a promising therapeutic candidate in the management of DN in humans. Further understanding of the molecular mechanisms of its neuromodulatory effects is essential in order to exploit its therapeutic efficacy.

Objective: The aim of this study was to analyze antioxidant effect of geraniol (GE) in different in vitro models.Methods: Initially, the antioxidant activity of GE was assessed by diphenyl picrylhydrazyl radical (DPPH) assay. The modulatory effect of GE against 2,2’-azobis(2-amidinopropane) dihydrochloride induced lipid peroxidation in rat brain regions (cortex and cerebellum) and sciatic nerve (SN) homogenates was determined. Further, the effect of GE was assessed against hyperglycemia-induced oxidative stress (OS) in SHSY5Y, a human neuroblastoma cell line.Results: GE proved to be a good scavenger of DPPH free radical (inhibitory concentration 50% [IC50] value = 663 nmol) and could lower the lipid peroxidation levels in rat brain tissue and SN homogenates (25-40%). Further, it rescue the SHSY5Y cells from hyperglycemia-induced death. Co-exposure of GE with the IC50 level of glucose (100 mM) lowered the levels of reactive oxygen species, hydrogen peroxides and 3-nitrotyrosine levels with concomitant elevation in the glutathione levels (about two folds).Conclusion: Collectively from these findings and other studies previously conducted (from our lab and others) emphasize the potential benefit of GE against OS, a progressive pathological feature of neurodegenerative disorders.

Catalase activities have been evaluated in testes and caput and cauda epididymis of Wistar rats fed on zinc deficient diet for 2 and 4 weeks. The enzyme activity has been measured as chromic acetate formed by heating of dichromate (in acetic acid) in presence of H2 O2 with perchromic acid as an unstable intermediate. Observed non-significant increase in catalase activity in testes as well as in caput and cauda epididymis of 2 weeks experiments has been related to low levels of H2 O2 produced in two organs whereas significant (P<0.01/0.001) increase in catalase activity in 4-weeks experiments indicate for increased oxidative stress due to phagocytotic activity of Sertoli cells in testes and damaged spermatozoa in epididymis. Thus, zinc deficiency increases catalase activity in testes and epididymis.