Srinivasan M.,Ayurveda Research Institute for Mother and Child Health Care |
Kalpana K.B.,Annamalai University |
Devipriya N.,Annamalai University |
Menon V.P.,Annamalai University
Biomedicine and Preventive Nutrition | Year: 2014
The present study was aimed to evaluate the radioprotective efficacy of lycopene, a naturally occurring dietary carotenoid on whole body radiation-induced cellular damage in the liver of Swiss albino mice. The first phase of the study was carried out to fix the effective concentration of lycopene by performing a 30 days survival studies using different graded doses (10, 20, 40 and 80. mg/kg body weight) of lycopene administered orally to mice via intragastric intubations for seven consecutive days prior to exposure of whole body radiation (10. Gy). Based on the results of survival studies, the effective dose of lycopene was fixed which was then administered to mice orally via intragastric intubations for 7 consecutive days prior to exposure of whole body radiation (4 Gy) to evaluate its radioprotective efficacy by performing various biochemical estimations, comet assay, DNA fragmentation assay and histopathological alterations in the liver of Swiss albino mice. The results indicated that radiation-induced decrease in the levels of endogenous antioxidant enzymes and increase in lipid peroxidative index, DNA damage and comet assays were altered by pre-administration with the effective dose of lycopene (20 mg/kg body weight) which restored the antioxidant status to near normal and decreased the levels of lipid peroxidative index, DNA damage and comet assays. These results were further confirmed by histopathological examinations, which indicated that pre-administration with the effective dose of lycopene reduced the hepatic damage induced by radiation. Thus the current study shows lycopene to be an effective radioprotector against radiation-induced damage in the liver of mice. © 2014.
Ai G.,South Dakota State University |
Dachineni R.,South Dakota State University |
Kumar D.R.,South Dakota State University |
Kumar D.R.,Central Institute of Brackishwater Aquaculture |
And 4 more authors.
Molecular Medicine Reports | Year: 2016
Glucose-6-phosphate dehydrogenase (G6PD) catalyzes the first reaction in the pentose phosphate pathway, and generates ribose sugars, which are required for nucleic acid synthesis, and nicotinamide adenine dinucleotide phosphate (NADPH), which is important for neutralization of oxidative stress. The expression of G6PD is elevated in several types of tumor, including colon, breast and lung cancer, and has been implicated in cancer cell growth. Our previous study demonstrated that exposure of HCT 116 human colorectal cancer cells to aspirin caused acetylation of G6PD, and this was associated with a decrease in its enzyme activity. In the present study, this observation was expanded to HT-29 colorectal cancer cells, in order to compare aspirin-mediated acetylation of G6PD and its activity between HCT 116 and HT-29 cells. In addition, the present study aimed to determine the acetylation targets of aspirin on recombinant G6PD to provide an insight into the mechanisms of inhibition. The results demonstrated that the extent of G6PD acetylation was significantly higher in HCT 116 cells compared with in HT-29 cells; accordingly, a greater reduction in G6PD enzyme activity was observed in the HCT 116 cells. Mass spectrometry analysis of aspirin-acetylated G6PD (isoform a) revealed that aspirin acetylated a total of 14 lysine residues, which were dispersed throughout the length of the G6PD protein. One of the important amino acid targets of aspirin included lysine 235 (K235, in isoform a) and this corresponds to K205 in isoform b, which has previously been identified as being important for catalysis. Acetylation of G6PD at several sites, including K235 (K205 in isoform b), may mediate inhibition of G6PD activity, which may contribute to the ability of aspirin to exert anticancer effects through decreased synthesis of ribose sugars and NADPH.
Marimuthu S.,Ayurveda Research Institute for Mother and Child Health Care |
Balakrishnan P.,Ayurveda Research Institute for Mother and Child Health Care |
Nair S.,Ayurveda Research Institute for Mother and Child Health Care
Pharmaceutical Biology | Year: 2013
Context: Melia azedarach Linn (Meliaceae) is an Ayurvedic medicinal plant which is native to India. It is traditionally used for the treatment of leprosy, inflammation, scrofula, anthelmintic, antilithic, diuretic, deobstruent and cardiac disorders. Objective: To evaluate the phytochemical constituents and antioxidant activities of the ethanol leaf extract of Melia azedarach (MA) and its protective effect against H2O2-induced cellular damage in cultured lymphocytes. Materials and methods: The dose-dependent study of MA (20, 40, 60, 80, 100 μg/ml) was used to study in vitro radical scavenging assays. The effective dose of MA (60 μg/ml) was further used to study the H2O2-induced DNA damage (comet assay and DNA fragmentation assay) in cultured lymphocytes. Results: The ethanol extract of MA (20, 40, 60, 80, 100 μg/ml) exhibited a significant dose-dependent inhibition of in vitro radical scavenging assays and their corresponding IC50 values as follows: hydroxyl radical (26.50 ± 0.26 μg/ml), superoxide anion (30.00 ± 0.32 μg/ml), nitric oxide radical (48.00 ± 0.48 μg/ml), DPPH radical (30.55 ± 0.32 μg/ml) and reducing power (22.00 ± 0.22 μg/ml). The increase in the severity of DNA damage and TBARS was increased significantly (p < 0.05) at 500 μM H2O 2-treated cultured lymphocytes and RBC cellular membranes. The phytochemical screening studies identified 13 chemical constituents present in the leaf extract of MA. Discussion and conclusion: The results of this study demonstrate that MA offers protection against H2O2-induced cellular damage and it can be developed as an effective antioxidant during oxidative stress. © 2013 Informa Healthcare USA, Inc. All rights reserved.
PubMed | Ayurveda Research Institute for Mother and Child Health Care
Type: Journal Article | Journal: Journal of basic and clinical physiology and pharmacology | Year: 2013
The present study aimed to evaluate the antihyperlipidemic effect of ferulic acid (FA) on carbon tetrachloride (CCl4)-treated rats.Female albino rats of the Wistar strain were used in the present study. The rats were divided into four groups: groups 1 and 4 received physiological saline (3 mL/kg body weight/week) by subcutaneous injection, whereas groups 2 and 3 received a subcutaneous injection of CCl4 (3 mL/kg body weight/week) for a total period of 12 weeks. In addition, groups 3 and 4 were administered FA (20 mL/kg body weight) every day for the last 90 days.The results showed significantly (p0.05) elevated levels of cholesterol, triglycerides (TG), and free fatty acids (FFA) in the liver and kidney of CCl4-treated rats as compared with those of the controls. In addition, the levels of cholesterol, FFA, phospholipids (PL), and TG were elevated significantly in the circulation. Administration of FA effectively reduced these levels of lipids in the plasma, liver, and kidney of CCl4-treated rats. The PL level was significantly decreased in the liver and kidney of CCl4-treated rats and was positively modulated by FA treatment. Our histopathological observations were also in correlation with the biochemical parameters.From the results obtained, we could conclude that FA effectively protects the system against hyperlipidemia and may be an effective therapeutic agent for the treatment of this disorder.