Novel action of vinpocetine in the prevention of paraquat-induced parkinsonism in mice: involvement of oxidative stress and neuroinflammation.

Parkinson's disease (PD) is a multifactorial chronic progressive neurodegenerative disease caused by age, genetic and environmental factors such as paraquat (PQT). PQT (a quartenary nitrogen herbicide) is implicated in some form of idiopathic PD. This study sought to investigate the protective effect of vinpocetine on paraquat-induced Parkinsonism in mice. Forty-eight male albino mice were randomly divided into 6 groups and treated orally as follows for 21 days; Group 1: vehicle normal (10 ml/kg), group 2: vehicle control (10 ml/kg); groups 3-5: vinpocetine (5, 10 or 20 mg/kg); group 6: vinpocetine (20 mg/kg). Animals in groups 2-5 were given PQT (10 mg/kg, i.p.) every 3 days for 3 weeks. The effect of treatments on spontaneous motor activity (open field test), muscle coordination (rotarod tests), cataleptic behaviour (bar test), and working memory (Y-maze test) were assayed. After the behavioural assay on day 21, the midbrain was isolated for estimation of oxidative stress and TNF-α. Intraperitoneal injection of paraquat significantly induced motor deficits, muscle incoordination, catalepsy and working memory impairment which was ameliorated by the pretreatment of mice with vinpocetine. In addition, paraquat injection caused marked increase in nitroso-oxidative stress markers with concomitant deficits in antioxidant enzymes activities (GSH and SOD) as well as induction of tumour necrotic factor-α (TNF-α) in the mid-brain which were attenuated by the pretreatment of mice with vinpocetine. Findings from this study showed that vinpocetine prevented paraquat-induced motor deficits, memory impairment, oxidative stress and neuroinflammation through enhancement of antioxidant defense system and inhibition of neuroinflammatory cytokine. Thus, could be a potential drug in the management of Parkinsonism.

The para isomer of dinitrobenzene disrupts redox homeostasis in liver and kidney of male wistar rats.

BACKGROUND: Para-Dinitrobenzene (p-DNB) is one of the isomers of dinitrobenzene which have been detected as environmental toxicants. Skin irritation and organ toxicities are likely for industrial workers exposed to p-DNB. This study evaluated the effect of sub-chronic exposure of rats to p-DNB on cellular redox balance, hepatic and renal integrity. METHODS: Forty eight male Wistar rats weighing 160-180 g were administered 50, 75, 1000 and 2000 mg/kg b.wt (body weight) of p-DNB or an equivalent volume of vehicle (control) orally and topically for 14 days. After the period of treatment, the activities of kidney and liver catalase (CAT), alkaline phosphatase (ALP) and superoxide dismutase (SOD) as well as extent of renal and hepatic lipid peroxidation (LPO) were determined. Serum ALP activity and plasma urea concentration were also evaluated. RESULTS: Compared with control animals, p-DNB -administered rats showed decrease in the body and relative kidney and liver weights as well as increased renal and hepatic hydrogen peroxide and lipid peroxidation levels accompanied by decreased superoxide dismutase and catalase activities. However, p-DNB caused a significant increase in plasma urea concentration and serum, liver and kidney ALP activities relative to control. In addition, p-DNB caused periportal infiltration, severe macro vesicular steatosis and hepatic necrosis in the liver. CONCLUSIONS: Our findings show that sub-chronic oral and sub-dermal administration of p-DNB may produce hepato-nephrotoxicity through oxidative stress.

Maternal and fetal indicators of oxidative stress during intrauterine growth retardation (IUGR).

The present study demonstrates the possibility of increased lipid peroxidation and protein oxidation in both maternal and fetal erythrocytes as markers of oxygen radical activity during intrauterine growth retardation. The erythrocyte MDA levels were significantly elevated in mothers of IUGR babies when compared to controls (p<0.01). The endogenous protein damage due to oxidative stress was significantly higher in IUGR mothers when compared to controls (p<0.05). Similarly the proteolytic activity in erythrocyte lysates against oxidatively damaged hemoglobin was significantly increased in mothers of IUGR babies compared to controls (p<0.001).In fetuses born with IUGR, both lipid peroxidation and proteolytic activity were significantly increased when compared to normal newborns (p<0.01).The result of this study indicates that oxidative stress was induced both in IUGR babies and their mothers which is manifested as increased lipid peroxidation and protein oxidant damage.

Status of salivary lipid peroxidation in oral cancer and precancer.

INTRODUCTION: Lipid oxidation gives rise to number of secondary by-products. Malondialdehyde (MDA) is the principal and most widely studied product of polyunsaturated fatty acid peroxidation. This aldehyde is a highly toxic molecule and should be considered as more than just a marker of lipid peroxidation in oral carcinogenesis. MATERIALS AND METHODS: Salivary malondiadldehyde was evaluated in 65 healthy controls (HC), 115 subjects with oral, potentially malignant disorders (PMD) and 50 subjects with oral squamous cell carcinoma (OSCC) using the Thiobarbituric-Trichloroacetitic acid (TBA-TCA) method. RESULTS: A consistent elevation in the levels of salivary MDA was observed in HC with tobacco related habits, subjects with PMD and subjects with OSCC. The elevation in the salivary MDA was significant (P = 0.001) in the groups PMD and OSCC and group OSCC when compared to HC. CONCLUSION: The significant and encouraging findings of this study thus validate and reinforce that salivary malodialdehyde analysis can be used as an efficient, noninvasive tool for the early diagnosis of PMD and OSCC for planning comprehensive treatment protocol.

Effect of cadmium-polluted water on plasma levels of tumor necrosis factor-α, interleukin-6 and oxidative status biomarkers in rats: protective effect of curcumin.

UNLABELLED: The present study was designed to investigate the effect of CdCl2-polluted drinking water (40 mg CdCl2/L) on the level of TNF-α and IL-6, as well as oxidative status biomarkers in plasma of rats. The possible protective effect of oral administration of curcumin (50 mg/kg body weight/day) was assessed. Results illustrated that Cd exposure significantly elevated the plasma levels of TNF-α and IL-6 (p<0.001) as compared to normal rats. Also, Cd administration resulted in a significant elevation in the lipid peroxidation and markedly reduction in the activities of SOD and catalase as well as the level of glutathione and total antioxidant capacity in plasma. The co-treatment of Cd with curcumin significantly reduced the levels of TNF-α and IL-6 and ameliorated the alteration in oxidative status biomarkers induced by Cd. Negative correlation between IL-6 or TNF-α was and the plasma activities of catalase, SOD and the level of total antioxidant capacity were found in rats exposed to Cd. CONCLUSION: Cadmium toxicity induced the release of TNF-α and IL-6 which is associated with systemic oxidative stress. This may be involved in the mechanism of the Cd toxicity. On the other hand, the findings suggest the curative action of curcumin against Cd toxicity.