Reaction-rate method for gamma-glutamyltransferase activity in serum.

Szasz, G

doi:10.1093/clinchem/22.12.2051

Cited by 142 publications

(49 citation statements)

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“…For the first 3 metabolites, commercially available fluorimetric assay kits were used (BioVision cat.# K354-100, K355-100 and K635-100) following the manufacturer's instructions. Phosphocreatine was measured according to a colorimetric assay 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 kit protocol described by Szas et al 25 . In total 96 metabolites including amine, acylcarnitines, organic acids, oxylipins and a number of nucleotides were measured.…”

Section: In Tissue Metabolome Analysismentioning

confidence: 99%

The Muscle Metabolome Differs between Healthy and Frail Older Adults

et al. 2016

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Populations around the world are aging rapidly. Age-related loss of physiological functions negatively affects quality of life. A major contributor to the frailty syndrome of aging is loss of skeletal muscle. In this study we assessed the skeletal muscle biopsy metabolome of healthy young, healthy older and frail older subjects to determine the effect of age and frailty on the metabolic signature of skeletal muscle tissue. In addition, the effects of prolonged whole-body resistance-type exercise training on the muscle metabolome of older subjects were examined. The baseline metabolome was measured in muscle biopsies collected from 30 young, 66 healthy older subjects, and 43 frail older subjects. Follow-up samples from frail older (24 samples) and healthy older subjects (38 samples) were collected after 6 months of prolonged resistance-type exercise training. Young subjects were included as a reference group. Primary differences in skeletal muscle metabolite levels between young and healthy older subjects were related to mitochondrial function, muscle fiber type, and tissue turnover. Similar differences were observed when comparing frail older subjects with healthy older subjects at baseline. Prolonged resistance-type exercise training resulted in an adaptive response of amino acid metabolism, especially reflected in branched chain amino acids and genes related to tissue remodeling. The effect of exercise training on branched-chain amino acid-derived acylcarnitines in older subjects points to a downward shift in branched-chain amino acid catabolism upon training. We observed only modest correlations between muscle and plasma metabolite levels, which pleads against the use of plasma metabolites as a direct read-out of muscle metabolism and stresses the need for direct assessment of metabolites in muscle tissue biopsies.

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Section: In Tissue Metabolome Analysismentioning

confidence: 99%

The Muscle Metabolome Differs between Healthy and Frail Older Adults

et al. 2016

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“…The activity of biochemical parameters such as aspartate transaminase (AST) and alanine transaminase (ALT) were estimated by the method of Reitman and Frankel. [25] Alkaline phosphatase (ALP) and g-glutamyl transferase (g-GT) were estimated by the methods of King [26] and Szasz [27] , respectively. Total bilirubin level was determined by a modified dimethyl sulfoxide (DMSO) method on the basis of sulfanilic acid reaction with sodium nitrite to produce deoxidized sulfanilic acid.…”

Section: Assessment Of Liver Injury Markers and Liver Tumour Markersmentioning

confidence: 99%

Chemopreventive evaluation of Tephrosia purpurea against N-nitrosodiethylamine-induced hepatocarcinogenesis in Wistar rats

Hussain

Siddiqui

Fareed

et al. 2012

Journal of Pharmacy and Pharmacology

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Objectives The chemopreventive potential of Tephrosia purpurea extract (TPE) on N‐nitrosodiethylamine (NDEA)‐induced hepatocellular carcinoma (HCC) in Wistar rats was assessed. Methods HCC was induced by a single intraperitoneal injection of NDEA (200 mg/kg) followed by subcutaneous injections of CCl4 (3 ml/kg per week) for six weeks. After administration of the carcinogen, 200 and 400 mg/kg TPE were administered orally once a day throughout the study. Key findings The levels of liver cancer markers, including α‐fetoprotein and carcinoembryonic antigen, were substantially increased by NDEA treatment. TPE treatment significantly reduced liver injury and restored the entire liver cancer markers. Additionally, TPE markedly normalized the activity of antioxidant enzymes, namely lipid peroxidation, reduced glutathione, catalase, superoxide dismutase, glutathione peroxidase and glutathione‐S‐transferase in the liver of NDEA‐treated rats. Treatment with TPE significantly reduced the nodule incidence and multiplicity in the carcinogen‐bearing rats. Histological observations of the liver tissues correlated with the biochemical observations. Conclusions These findings powerfully support that T. purpurea prevented lipid peroxidation, suppressed the tumour burden, and promoted enzymatic and nonenzymatic antioxidant defence systems during NDEA‐induced hepatocarcinogenesis. This might have been due to modulating the antioxidant defence status, which contributed to its anticarcinogenic potential.

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“…Serum. Spectrophotometric kinetic methods were used to determine the activity of AST, 36 ALT, 36 ALP, 37 c-GT, 38 SDH, 39 GDH, 40 as well as the serum concentrations of AcAc and b-GB. 41 All of the aforementioned activities and concentrations were measured at 30uC.…”

Section: Biochemical Analysismentioning

confidence: 99%