A colorimetric method for the determination of serum glutamic oxalacetic and glutamic pyruvic transaminases.
01 Jul 1957-American Journal of Clinical Pathology (AMERICAN JOURNAL OF CLINICAL PATHOLOGY)-Vol. 28, Iss: 1, pp 56-63
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TL;DR: Treatment with (PhSe)2 after APAP administration can reverse the neurotoxicity caused by a single toxic dose of APAP, and the neuroprotective effect of (Ph Se)2 is likely associated with its antioxidant properties.
Abstract: Organoselenium compounds exhibit antioxidant activity, as well as a variety of biological activities, with potential pharmacological and therapeutic applications. The aim of this study was to investigate the effect of diphenyl diselenide (PhSe)2 in reversing oxidative brain damage and mitochondrial dysfunction caused by administration of acetaminophen (APAP) in mice. Mice received a toxic dose of APAP, followed by a dose of (PhSe)2 1 h later. Four hours after the administration of APAP, plasma was withdrawn from the mice and used for biochemical assays of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) as markers of hepatotoxicity. Brain homogenate was examined to determine oxidative stress. Isolated brain mitochondria were examined to quantify mitochondrial transmembrane's electrical potential and mitochondrial swelling and to estimate reactive oxygen species (ROS) production. APAP administration caused an increase in plasma ALT and AST activities. APAP administration also caused a significant increase in the levels of thiobarbituric acid reactive substances (TBARS) and dichlorofluorescein oxidation in brain homogenate. Similarly, mitochondrial swelling and ROS production increased after APAP administration. APAP treatment also caused a decrease in Na+ , K+ - ATPase activity and in mitochondrial membrane potential. These alterations observed in the brain of APAP-treated mice were restored by (PhSe)2. Glutathione levels were decreased by APAP, but (PhSe)2 did not reverse this change. Treatment with (PhSe)2 after APAP administration can reverse the neurotoxicity caused by a single toxic dose of APAP. The neuroprotective effect of (PhSe)2 is likely associated with its antioxidant properties.
68 citations
Cites methods from "A colorimetric method for the deter..."
...Transaminases were determined by the colorimetric method of Reitman and Frankel (1957)....
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TL;DR: Oral administration of alcoholic extracts of Schouwia thebica Webb showed that extracts are safe for human use, and the studied extracts are considered safe, since they failed to induce death of mice in doses up to 4000 mg/kg body weight.
68 citations
TL;DR: Glycylprolyl β-naphthylamidase activities in sera from 40 normal subjects (18–81 years) were 22.6 ± 0.9 (S.E.) (11.8–38.2) I.U./l serum at 37°C, and the enzyme activities did not differ significantly with age between the younger group under 40-years-old and the older group over 40- years-old.
68 citations
TL;DR: The results prove that AGE has antioxidant and protective effects against CP-induced oxidative stress and changes in parameters of blood cells and liver structure in rats, and could be used as a dietary supplementation to reduce toxic side effects of anticancer drugs.
Abstract: Cisplatin (CP) is one of the most active cytotoxic drugs. However, it has several side effects that are associated with increased oxidative stress. Aged garlic extract (AGE) is a natural product containing different compounds with antioxidant activity. The present study aimed to evaluate the effect of AGE on CP-induced hepatotoxicity. Four equally male rat groups: control, AGE-treated (250 mg/kg once for 21 days), CP-treated (7.5 mg/kg, once intraperitoneal), combined AGE and CP-treated were used. Blood samples were collected to investigate blood picture and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin (TSB) and albumin. The liver of each rat was excised, cleaned, weighed, rinsed in ice-cold saline and homogenized for assessment malondialdehyde (MDA) level, catalase (CAT) and superoxide dismutase (SOD) activities and level of reduced glutathione (GSH). Histological examination was also carried out. AGE-pretreated rats revealed significant reduction in serum levels of AST, ALT & TSB and increase serum albumin level induced by CP administration. Furthermore, AGE significantly ameliorated CP-induced increase in MDA level and decrease in GSH level, CAT and SOD activities in liver tissue homogenates. Additionally, histopathological and blood picture examinations revealed markedly ameliorated CP-induced toxicity on blood cells parameters and liver structure. Our results prove that AGE has antioxidant and protective effects against CP-induced oxidative stress and changes in parameters of blood cells and liver structure in rats. Thus, it could be used as a dietary supplementation to reduce toxic side effects of anticancer drugs.
68 citations
TL;DR: Experimental results suggest that AA protects arsenic-induced cytotoxicity in murine hepatocytes, and the cytoprotective activity of AA was found to be comparable to that of a known antioxidant, vitamin C.
67 citations