University of Madras

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.

Consistency of spin-1 theories in external electromagnetic fields

Abstract: It is known that while spin-1 (Proca) theory with minimal electromagnetic interaction is marred by the Corben-Schwinger anomaly, the inclusion of specific types of 'anomalous' interactions lead to other difficulties such as non-causality of propagation, and the energy spectrum (in homogeneous magnetic fields of sufficient strength) becoming partially non-real The authors investigate whether, by making the anomalous terms (introduced into the Duffin-Kemmer-Petiau equation) sufficiently general, it is possible to escape these inconsistencies The answer, unfortunately, turns out to be in the negative They comment briefly on other formulations for spin-1

Mitigation of oxidative stress in cyclophosphamide-challenged hepatic tissue by DL-α-lipoic acid

Abstract: The present study investigated the protective effect of DL-alpha-lipoic acid on the tissue peroxidative damage and abnormal antioxidant levels in cyclophosphamide (CP) induced hepatotoxicity. Male Wistar rats of 140 +/- 20 g were categorized into four groups. Two groups were administered CP (15 mg/kg body weight once a week for 10 weeks by oral gavage) to induce hepatotoxicity; one of these groups received lipoic acid treatment (35 mg/kg body weight intraperitoneally once a week for 10 weeks; 24 h prior to the CP administration). A vehicle (saline) treated control group and a lipoic acid drug control group were also included. The extent of liver damage in CP-induced rats was evident from the increased activities of serum aminotransferases, alkaline phosphatase and lactate dehydrogenase; whereas lipoic acid pretreatment prevented the rise in these marker enzymes. We evaluated the changes in activities/levels of tissue enzymic (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glucose-6-phosphate dehydrogenase) and non-enzymic (reduced glutathione, ascorbate and a-tocopherol) antioxidants along with malondialdehyde levels in the experimental groups. In CP-administered rats the antioxidant enzymes showed significantly depressed activities (p < 0.001, p < 0.01) and the antioxidant molecules also showed depleted levels (p < 0.001, p < 0.01), in comparison with the control group. However the extent of lipid peroxidation and the abnormal antioxidant status were normalized in lipoic acid pretreated rats. The present work highlights the efficacy of lipoic acid as a cytoprotectant in CP-induced hepatic oxidative injury.

Targeting of DNA molecules, BSA/c-Met tyrosine kinase receptors and anti-proliferative activity of bis(terpyridine)copper(II) complexes

Abstract: A series of homoleptic bis(terpyridine)copper(II) complexes of the type [Cu(L1–5)2]Cl2 (1–5), where L1–5 = 4′-(4-substituted)-2,2′:6′,2′′-terpyridines, have been synthesized and characterized. The molecular structure of complex 2 was confirmed by the single crystal XRD technique, and the geometry of the complexes is best described as distorted octahedral. Structural parameters from the crystallographic and DFT studies are in good agreement with each other. The small HOMO–LUMO energy gap supports bioefficacy of the complexes. DNA binding studies show high intrinsic binding constant values 1.53 ± 0.15, 1.62 ± 0.08 and 3.09 ± 0.12 × 105 M−1 for complexes 1, 2 and 3, respectively, with intercalative mode of binding to CT-DNA. The binding results were further supported by molecular docking studies. The experimental results indicate that the interaction between the complexes and BSA protein involves a static quenching mechanism. The molecular docking studies with c-Met tyrosine kinase receptors show hydrophobic and π–π interactions. All the complexes bring about hydroxyl radical mediated DNA cleavage in the presence of H2O2. In vitro cytotoxicities of the complexes (1–3) were tested against three cancerous cell lines, namely human breast adenocarcinoma (MCF-7), epithelioma (Hep-2) and cervical (HeLa) cell lines, and one non-tumorigenic human dermal fibroblast (NHDF) cell line by MTT reduction assay. The morphological assessment data obtained using Hoechst 33258 staining revealed that complex 3 induces apoptosis much more effectively than the other complexes.

Effect of tamoxifen on lipid peroxide and antioxidative system in postmenopausal women with breast cancer.

Abstract: Background. Current evidence clearly indicates that free radicals play a prominent role in the incidence and development of breast cancer. Available literature suggests that tamoxifen is a potent suppressor of lipid peroxide formation in both animal and human systems. The purpose of this study was to understand the rate of lipid peroxidation and the status of antioxidants in tamoxifen-treated postmenopausal women with breast cancer. Methods. A short term evaluation of 6 months' tamoxifen therapy (10 mg twice a day) in 64 postmeno-pausal women was conducted. The rate of serum lipid peroxidation and the status of enzymic and nonenzymic antioxidants were evaluated before and after 3 and 6 months' tamoxifen treatment. Results. At 3 and 6 months' evaluation, tamoxifen-treated patients showed a significantly decreased concentration of malondialdehyde (P < 0.001), an end product of lipid peroxidation, and remarkably increased levels of enzymic and nonenzymic antioxidants. In addition to that, the concentrations of serum selenium and vitamins A, C, and E were increased significantly (P < 0.01 for each) in these patients. Conclusion. The results suggest that tamoxifen therapy exerts significant positive effects on the rate of lipid peroxidation and protective systems in postmenopausal women with breast cancer.