Browsing by Author "Vijayakaran, Karunakaran"
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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 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.OtherItem Open Access Protective Action Of Curcumin and Nano-Curcumin against Arsenic-Induced Genotoxicity In Rats In Vivo(TANUVAS, Chennai, 2014-12) Sankar, P.; Senthilkumar, P.; Ranganathan, V.; Telang, Avinash Gopal; Ramya, K.; Vijayakaran, Karunakaran; Kesavan, Manickam; Sarkar, Souvendra NathWe explored whether nanoformulation of curcumin can cause better protective effect than free curcumin against arsenic-induced genotoxicity. Curcurnin- loaded Poly (lactic-co-glycolic acid) nanoparticles (CUR-NP) were prepared by emulsion technique. The CUR-NPwere water soluble and showed biphasic release pattern.Rats was divided into 5 groups of 6 each.