Browsing by Author "Sankar, Palanisamy"
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ArticleItem Open Access Arsenic decreases antinociceptive activity of paracetamol: Possible involvement of serotonergic and endocannabinoid receptors(Elsevier, 2014) Vijayakaran, Karunakaran; Kesavan, Manickam; Kannan, Kandasamy; Sankar, Palanisamy; Tandan, Surendra Kumar; Sarkar, Souvendra Nath; TANUVASWe assessed whether repeated arsenic exposure can decrease paracetamol-mediated antinociception by modulating serotonergic and endocannabinoid pathways. Rats were preexposed to elemental arsenic (4 ppm) as sodium arsenite through drinking water for 28 days. Next day paracetamol’s (400 mg/kg, oral) antinociceptive activity was assessed through formalin-induced nociception. Serotonin content and gene expression of 5-HT1A, 5-HT2A and CB1 receptors were evaluated in brainstem and frontal cortex. Arsenic decreased paracetamol-mediated analgesia. Paracetamol, but not arsenic, increased serotonin content in these regions. Arsenic attenuated paracetamol-mediated increase in serotonin level. Paracetamol did not alter 5-HT1Aexpression, but caused down-regulation of 5-HT2Aand up-regulation of CB1 receptors. Arsenic down-regulated these receptors. However,paracetamol-mediated down-regulation of 5-HT2Awas more pronounced. Arsenic did not modify paracetamol’s effect on 5-HT1A expression, but reduced paracetamol - mediated down - regulation of 5-HT2A and reversed up-regulation of CB1 receptors. Results suggest arsenic reduced paracetamol-induced analgesia possibly by interfering with pronociceptive 5-HT2A and antinociceptive CB1 receptors.ArticleItem Open Access Arsenic reduces the antipyretic activity of paracetamol in rats: Modulation of brain COX-2 activity and CB1 receptor expression(Elsevier, 2014) Vijayakaran, Karunakaran; Kannan, Kandasamy; Kesavan, Manickam; Suresh, Subramaniyam; Sankar, Palanisamy; Tandan, Surendra Kumar; Sarkar, Souvendra Nath; TANUVAStWe examined whether subacute arsenic exposure can reduce paracetamol-mediatedantipyretic activity by affecting COX pathway and cannabinoid CB1receptor regulation.Rats were preexposed to elemental arsenic (4 ppm) as sodium arsenite through drinkingwater for 28 days. Next day pyrexia was induced with lipopolysaccharide and paraceta-mol’s (200 mg/kg, oral) antipyretic activity was assessed. The activities of COX-1 and COX-2,the levels of PGE2, TNF- and IL-1 and expression of CB1receptors were assessed in brain.Arsenic inhibited paracetamol-mediated antipyretic activity. COX-1 activity was not affectedby any treatments. Paracetamol decreased COX-2 activity, levels of PGE2, TNF- and IL-1 andcaused up-regulation of CB1receptors. Arsenic caused opposite effects on these parameters.In the arsenic-preexposed rats, paracetamol-mediated effects were attenuated, while CB1receptor up-regulation was reversed to down-regulation. Results suggest that elevated COX-2 activity and reduced CB1expression could be involved in the arsenic-mediated attenuationof the antipyretic activity of paracetamol.ArticleItem Open Access Atorvastatin restores arsenic-induced vascular dysfunction in rats: Modulation of nitric oxide signaling and inflammatory mediators(Elsevier, 2014) Kesavan, Manickam; Sasindran Sarath, Thengumpallil; Kannan, Kandasamy; Suresh, Subramaniyam; Gupta, Priyanka; Vijayakaran, Karunakaran; Sankar, Palanisamy; Kurade, Nitin Pandurang; Mishra, Santosh Kumar; Sarkar, Souvendra Nath; TANUVASWe evaluated whether atorvastatin, an extensively prescribed statin for reducing the risks of cardiovascular diseases, can reduce the risk of arsenic-induced vascular dysfunction and inflammation in rats and whether the modulation could be linked to improvement in vascular NO signaling. Rats were exposed to sodium arsenite (100 ppm)through drinkingwater for 90 consecutive days. Atorvastatin (10 mg/kgbw, orally)was administered once daily during the last 30 days of arsenic exposure. On the 91st day, blood was collected for measuring serum C-reactive protein. Thoracic aorta was isolated for assessing reactivity to phenylephrine, sodium nitroprusside and acetylcholine; evaluating eNOS and iNOS mRNA expression and measuring NO production,while abdominal aorta was used for ELISA of cytokines, chemokine and vascular cell adhesionmolecules. Histopathologywas done in aortic arches. Arsenic did not alter phenylephrine-elicited contraction. Atorvastatin inhibited Emax of phenylephrine, but it augmented the contractile response in aortic rings from arsenic-exposed animals. Sodium nitroprusside-induced relaxation was not altered with any treatment. However, arsenic reduced acetylcholineinduced relaxation and affected aortic eNOS at the levels of mRNA expression, protein concentration, phosphorylation and NO production. Further, it increased aortic iNOS mRNA expression, iNOS-derived NO synthesis, production of pro-inflammatory mediators (IL-1β, IL-6, MCP-1, VCAM, sICAM) and serum C-reactive protein and aortic vasculopathic lesions. Atorvastatin attenuated these arsenic-mediated functional, biochemical and structural alterations. Results show that atorvastatin has the potential to ameliorate arsenic-induced vascular dysfunction and inflammation by restoring endothelial function with improvement in NO signaling and attenuating production of pro-inflammatory mediators and cell adhesion molecules.ArticleItem Open Access Effects of Nanoparticle-Encapsulated Curcumin on Arsenic-Induced Liver Toxicity in Rats(Wiley Periodicals, Inc., 2013) Sankar, Palanisamy; Telang, Avinash Gopal; Kalaivanan, Ramya; Karunakaran, Vijayakaran; Kesavan, Manickam; Sarkar, Souvendra Nath; TANUVASWe investigated the therapeutic effectiveness of the nanoparticle-encapsulated curcumin (CUR-NP) against sodium arsenite-induced hepatic oxidative damage in rats. The CUR-NP prepared by emulsion technique was spherical in shape with an encapsulation efficiency of 86.5%. The particle size ranged between 120 and 140 nm with the mean particle size being 130.8 nm. Rats were divided into five groups of six each. Group 1 served as control. Group 2 rats were exposed to sodium arsenite (25 ppm) daily through drinking water for 42 days. Groups 3, 4, and 5 were treated with arsenic as in group 2, however, they were administered, empty nanoparticles, curcumin (100 mg/kg bw) and CUR-NP (100 mg/kg bw), respectively, by oral gavage during the last 14 days of arsenic exposure. Arsenic increased the activities of serum alanine aminotransferase and aspartate aminotransferase and caused histological alterations in liver indicating hepatotoxicity. Arsenic increased lipid peroxidation, depleted reduced glutathione and decreased the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in liver. All these effects of arsenic were attenuated with both curcumin and CUR-NP. However, the magnitude of amelioration was more pronounced with CUR-NP. The results indicate that curcumin given in nano-encapsulated form caused better amelioration than free curcuminArticleItem Open Access Oral nanoparticulate curcumin combating arsenic-induced oxidative damage in kidney and brain of rats(SAGE Publications, 2013) Sankar, Palanisamy; Telang, Avinash Gopal; Kalaivanan, Ramya; Karunakaran, Vijayakaran; Suresh, Subramaniyam; Kesavan, Manickam; TANUVASArsenic exposure through drinking water causes oxidative stress and tissue damage in the kidney and brain. Curcumin (CUR) is a good antioxidant with limited clinical application because of its hydrophobic nature and limited bioavailability, which can be overcome by the encapsulation of CUR with nanoparticles (NPs). The present study investigates the therapeutic efficacy of free CUR and NP-encapsulated CUR (CUR-NP) against sodium arsenite-induced renal and neuronal oxidative damage in rat. The CUR-NP prepared by emulsion tech- nique and particle size ranged between 120 and 140 nm, with the mean particle size being 130.8 nm. Rats were divided into five groups (groups 1–5) with six animals in each group. Group 1 served as control. Group 2 rats were exposed to sodium arsenite (25 ppm) daily through drinking water for 42 days. Groups 3, 4, and 5 were treated with arsenic as in Group 2; however, these animals were also administered with empty NPs, CUR (100 mg/kg body weight), and CUR-NP (100 mg/kg), respectively, by oral gavage during the last 14 days of arsenic exposure. Arsenic exposure significantly increased serum urea nitrogen and creatinine levels. Arsenic increased lipid peroxidation (LPO), reduced glutathione content and the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were depleted significantly in both kidney and brain. Treatment with free CUR and CUR-NP decreased the LPO and increased the enzymatic and nonenzymatic antioxidant system in kidney and brain. Histopathological examination showed that kidney and brain injury mediated by arsenic was ameliorated by treatment. However, the amelioration percentage indicates that CUR-NP had marked therapeutic effect on arsenic-induced oxidative damage in kidney and brain tissues.ArticleItem Open Access Protective action of curcumin and nano-curcumin against arsenic- induced genotoxicity in rats in vivo(Springer, 2014-07) Sankar, Palanisamy; Telang, Avinash Gopal; Ramya, Kalaivanan; Vijayakaran, Karunakaran; Kesavan, Manickam; Sarkar, Souvendra Nath; TANUVASenite (25 ppm) daily through drinking water for 42 days. Groups III, IV and V were maintained as in Group II, however, they were also administered empty nanoparticle, curcumin (100 mg/kg bw) and CUR-NP (100 mg/kg bw), respec- tively, by oral gavage during the last 14 days of arsenic exposure. On the 43rd day, genotoxic effects were evalu- ated in bone marrow cells. Arsenic increased chromosomal aberrations, micronuclei formation and DNA damage. Both free curcumin and CUR-NP attenuated these arsenic- mediated genotoxic effects. However, the result suggests that nanoformulation have better protective effect than free curcumin at the same dose level.