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Institution

University of Madras

EducationChennai, Tamil Nadu, India
About: University of Madras is a education organization based out in Chennai, Tamil Nadu, India. It is known for research contribution in the topics: Ring (chemistry) & Lipid peroxidation. The organization has 8496 authors who have published 11369 publications receiving 211152 citations. The organization is also known as: Madras University & University of Chennai.


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Journal ArticleDOI
TL;DR: Increased levels of phosphate, nitrite, nitrate, silicate, organic matter and organic carbon during the post monsoon reduce the bioavailability of mercury by forming complexes which may increase the concentration of mercury in the sediments during postmonsoon.

82 citations

Journal ArticleDOI
TL;DR: G gestational DEHP exposure predisposes F1 offspring to glucometabolic dysfunction at adulthood by down-regulating the expression of critical genes involved in the insulin signalling pathway, and DEHP-induced epigenetic alterations in Glut4 appear to play a significant role in disposition towards this metabolic abnormality.
Abstract: Di-(2-ethylhexyl)phthalate (DEHP) is an endocrine-disrupting chemical (EDC), widely used as a plasticiser. Developmental exposure to EDCs could alter epigenetic programming and result in adult-onset disease. We investigated whether DEHP exposure during development affects glucose homoeostasis in the F1 offspring as a result of impaired insulin signal transduction in gastrocnemius muscle. Pregnant Wistar rats were administered DEHP (0, 1, 10 and 100 mg/kg per day) from embryonic days 9-21 orally. DEHP-exposed offspring exhibited elevated blood glucose, impaired serum insulin, glucose tolerance and insulin tolerance, along with reduced insulin receptor, glucose uptake and oxidation in the muscle at postnatal day 60. The levels of insulin signalling molecules and their phosphorylation were down-regulated in DEHP-exposed offspring. However, phosphorylated IRS1(Ser636/639), which impedes binding of downstream effectors and the negative regulator (PTEN) of PIP3, was increased in DEHP-exposed groups. Down-regulation of glucose transporter 4 (Glut4 (Slc2a4)) gene expression and increased GLUT4(Ser488) phosphorylation, which decreases its intrinsic activity and translocation towards the plasma membrane, were recorded. Chromatin immunoprecipitation assays detected decreased MYOD binding and increased histone deacetylase 2 interaction towards Glut4, indicative of the tight chromatin structure at the Glut4 promoter. Increased DNMTs and global DNA methylation levels were also observed. Furthermore, methylation of Glut4 at the MYOD-binding site was increased in DEHP-exposed groups. These findings indicate that, gestational DEHP exposure predisposes F1 offspring to glucometabolic dysfunction at adulthood by down-regulating the expression of critical genes involved in the insulin signalling pathway. Furthermore, DEHP-induced epigenetic alterations in Glut4 appear to play a significant role in disposition towards this metabolic abnormality.

82 citations

Journal ArticleDOI
TL;DR: In this paper, a solvent-free composite polymer electrolyte consisting of poly(ethylene oxide) (PEO) incorporated into diphenyl amine (DPA) along with KI and I 2 has been developed.

82 citations

Journal ArticleDOI
TL;DR: The findings suggest that the oral treatment with RA alleviates pancreatic β-cell dysfunction and glucolipotoxicity-mediated oxidative stress during HFD-STZ-induced type 2 Diabetes (T2DM), perhaps through its antioxidant potential.
Abstract: Persistent hyperglycemia and elevated levels of free fatty acids (FFA) contribute to oxidative stress, a proximate cause for the onset and progression of diabetes and its complications. The present study was hypothesized to evaluate the anti-diabetic potential of Rosmarinic acid (RA) during high-fat diet (HFD)—streptozotocin (STZ)-induced type 2 Diabetes (T2D) in wistar albino rats. Oral administration of RA (100 mg/kg b.w) significantly (p < 0.05) increased the insulin sensitivity index (ISI0,120), while the levels of blood glucose, HbA1c, advanced glycation end products (AGE), TNF-α, IL-1β, IL 6, NO, p-JNK, P38 MAPK and NF-κB were significantly reduced, with a concomitant elevation in the plasma insulin levels in diabetic rats. Furthermore, RA treatment significantly (p < 0.05) reduced the levels of triglycerides, FFA and cholesterol in serum, and reduced the levels of lipid peroxides, AOPP’s and protein carbonyls in the plasma and pancreas of diabetic rats. The diminished activities of pancreatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) and the decreased levels of plasma ceruloplasmin, vitamin C, vitamin E and reduced glutathione (GSH) in diabetic rats were also significantly (p < 0.05) recovered upon RA treatment denoting its antioxidant potential which was confirmed by Nrf-2, hemeoxyenase (HO-1) levels. Histological, ultrastructural and immunohistochemical data demonstrate that oral administration of RA protects pancreatic β-cells from oxidative niche in HFD-STZ-induced experimental diabetes. Our findings suggest that the oral treatment with RA alleviates pancreatic β-cell dysfunction and glucolipotoxicity-mediated oxidative stress during HFD-STZ-induced T2DM, perhaps through its antioxidant potential.

82 citations

Journal ArticleDOI
TL;DR: The significantly elevated plasma levels of TNF-alpha found in arthritic rats were found to be significantly restored back to near normal levels by the extract of C. gynandra extract, and the membrane stabilizing activity of the extract was further evidenced by histological observations made on the limb tissue.

82 citations


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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202315
202283
2021644
2020564
2019457
2018435