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
About: This article is published in American Journal of Clinical Pathology.The article was published on 1957-07-01. It has received 9424 citations till now.
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TL;DR: Data from this study suggest for the first time that carnitine deficiency is a risk factor and could precipitate cisplatin-induced hepatotoxicity, and propionyl-l-carnitine prevents the development of cisplant-induced liver injury.
Abstract: This study investigates whether or not carnitine deficiency is a risk factor and could contribute to cisplatin-induced liver toxicity. A total of 60 adult male Wistar albino rats were divided into six groups. The first three groups were injected intraperitoneally with normal saline, propionyl-l-carnitine (500 mg/kg), and d-carnitine (500 mg/kg), respectively, for 10 successive days. The fourth, fifth and sixth groups were injected intraperitoneally with the same doses of normal saline, propionyl-l-carnitine and d-carnitine, respectively, for 5 successive days before and after a single dose of cisplatin (7 mg/kg). Administration of the standard nephrotoxic dose of cisplatin did not produce any changes in serum alanine transaminase and gamma-glutamyl transferase and no morphological changes in liver tissues. However, it did produce a significant increase in thiobarbituric acid reactive substances and total nitrate/nitrite and a significant decrease in reduced glutathione content in liver tissues. On the other hand, combined treatment with cisplatin and d-carnitine induced a dramatic increase in serum alanine transaminase and gamma-glutamyl transferase, as well as progressive reduction in total carnitine and ATP content in liver tissue. Moreover, histopathological examination of liver tissues confirmed the biochemical data, where cisplatin and d-carnitine combination showed signs of liver injury manifested as focal necro-inflammatory changes and portal inflammation. Interestingly, in carnitine supplemented rats using propionyl-l-carnitine, cisplatin did not produce any biochemical and histopathological changes in liver tissues. In conclusion, data from this study suggest for the first time that (1) carnitine deficiency is a risk factor and could precipitate cisplatin-induced hepatotoxicity, (2) oxidative stress is not the main cause of cisplatin-related hepatotoxicity and (3) propionyl-l-carnitine prevents the development of cisplatin-induced liver injury.
55 citations
TL;DR: The results herein demonstrate the toxic effects of AFB1 in O. niloticus, and the observed alterations in fish status, especially in the liver coincide well with the expected oxidative stress resulting from the AFB1 toxicity.
Abstract: Aflatoxin is a common contaminant of foods, particularly in the staple diets of many developing countries. To evaluate adverse effects of aflatoxin B1 (AFB1) toxicity on health status in the Nile tilapia Oreochromis niloticus, fish were fed diet contaminated with either 20 or 100 ppb AFB1 for 6 or 12 weeks. Growth indices, survival rate and hepatosomatic index (HSI) were assessed. Blood samples were collected for hematological profiles (e.g. RBCs and WBC count, Hb content). Liver enzyme activity; aspartate aminotransferase (AST), alanine aminotransferase (ALT) as well as alkaline phosphatase (ALP), were evaluated and toxin residues in the liver and musculature were detected. Liver histopathological investigations were carried out, whereas antioxidant glutathione peroxidase (GPx) and glutathione S-transferase (GST) gene expression were determined in this tissue by semi-quantitative RT-PCR. Furthermore, to test the fish immune status, challenge against Aeromonas hydrophila was conducted. Results indicated that 100 ppb AFB1 negatively impacted O. niloticus weight gain, feed efficiency, hematological profiles, HSI as well as liver histopathology, while increase in AST, ALT, ALP liver enzymes activity was evidenced. Further, the expression of liver GPx and GST down-regulated and AFB1 residues were always detected in the liver and only in the musculature in fish fed 100 ppb AFB1 for 12 weeks. The ability of fish to withstand A. hydrophila infection was remarkably lowered. Overall, the results herein demonstrate the toxic effects of AFB1 in O. niloticus. The observed alterations in fish status, especially in the liver coincide well with the expected oxidative stress resulting from the AFB1 toxicity.
55 citations
TL;DR: Relationships between growth rate, protein content, transaminases, and phosphatases provided strong evidence for the involvement of pesticidal contamination in the biochemical changes in earthworms, which can be used as a bioindicator of soil contamination by pesticides.
Abstract: This study was conducted to investigate the toxicity of aldicarb, cypermethrin, profenofos, chlorfluazuron, atrazine, and metalaxyl toward mature Aporrectodea caliginosa earthworms. The effects of the LC25 values of these pesticides on the growth rate in relation to glucose, soluble protein, and activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT), acid phosphatase (AcP), and alkaline phosphatase (AIP) were also studied. The results showed that aldicarb was the most toxic of the tested pesticides, followed in order by cypermethrin, profenofos, chlorfluazuron, atrazine, and metalaxyl. A reduction in growth rate was observed in all pesticide-treated worms, which was accompanied by a decrease in soluble protein and an increase in transaminases and phosphatases. Relationships between growth rate, protein content, transaminases, and phosphatases provided strong evidence for the involvement of pesticidal contamination in the biochemical changes in earthworms, which can be used as a bioindicator of soil contamination by pesticides. © 2003 Wiley Periodicals, Inc. Environ Toxicol 18: 338–346, 2003.
55 citations
TL;DR: Chronic BDL significantly increased most of plasma and hepatic cytokine levels and diminished the hepatic IFN-gamma amount and NO was increased in both tissues, but such change was only significant in plasma.
55 citations
TL;DR: Four compounds forming metabolic intermediate complexes with cytochrome P-450 in vitro were studied for their effects on hepatic glutathione in the mouse and their depletion was transient for piperonyl butoxide and SKF 525-A while lasting at least 24 hr for other compounds.
55 citations