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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
medicine
Progression of diethylnitrosamine-induced hepatic carcinogenesis in carnitine-depleted rats
World Journal of Gastroenterology, Volume 15, No. 11, Year 2009
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Description
Aim: To investigate whether carnitine deficiency is a risk factor during the development of diethylnitrosamine (DENA)-induced hepatic carcinogenesis. Methods: A total of 60 male Wistar albino rats were divided into six groups with 10 animals in each group. Rats in group 1 (control group) received a single intraperitoneal (i.p.) injection of normal saline. Animals in group 2 (carnitine-supplemented group) were given L-carnitine (200 mg/kg per day) in drinking water for 8 wk. Animals in group 3 (carnitine-depleted group) were given D-carnitine (200 mg/kg per day) and mildronate (200 mg/kg per day) in drinking water for 8 wk. Rats in group 4 (DENA group) were injected with a single dose of DENA (200 mg/ kg, i.p.) and 2 wk later received a single dose of carbon tetrachloride (2 mL/kg) by gavage as 1:1 dilution in corn oil. Animals in group 5 (DENA-carnitine depleted group) received the same treatment as group 3 and group 4. Rats in group 6 (DENA-carnitine supplemented group) received the same treatment as group 2 and group 4. Results: Administration of DENA resulted in a significant increase in alanine transaminase (ALT), gamma-glutamyl transferase (G-GT), alkaline phosphatase (ALP), total bilirubin, thiobarbituric acid reactive substances (TBARS) and total nitrate/nitrite (NOx) and a significant decrease in reduced glutathione (GSH), glutathione peroxidase (GSHPx), catalase (CAT) and total carnitine content in liver tissues. In the carnitine-depleted rat model, DENA induced a dramatic increase in serum ALT, G-GT, ALP and total bilirubin, as well as a progressive reduction in total carnitine content in liver tissues. Interestingly, L-carnitine supplementation resulted in a complete reversal of the increase in liver enzymes, TBARS and NOx, and a decrease in total carnitine, GSH, GSHPx, and CAT induced by DENA, compared with the control values. Histopathological examination of liver tissues confirmed the biochemical data, where L-carnitine prevented DENA-induced hepatic carcinogenesis while D-carnitine-mildronate aggravated DENA-induced hepatic damage. Conclusion: Data from this study suggest for the first time that: (1) carnitine deficiency is a risk factor and should be viewed as a mechanism in DENA-induced hepatic carcinogenesis; (2) oxidative stress plays an important role but is not the only cause of DENA-induced hepatic carcinogenesis; and (3) long-term L-carnitine supplementation prevents the development of DENA-induced liver cancer. © 2009 The WJG Press and Baishideng. All rights reserved.
Authors & Co-Authors
Al-Rejaie, Salim Salih
Saudi Arabia, Riyadh
King Saud University
Aleisa, Abdulaziz Mohamed A.
Saudi Arabia, Riyadh
King Saud University
al-Yahya, Abdulaziz Abdulrhman
Saudi Arabia, Riyadh
King Saud University
Bakheet, Saleh Abdulrahman I.
Saudi Arabia, Riyadh
King Saud University
AlSheikh, Abdulmalik M.
Saudi Arabia, Riyadh
King Saud University
Fatani, Amal Jamil Y.
Saudi Arabia, Riyadh
King Saud University
Al-Shabanah, Othman Abdualla
Saudi Arabia, Riyadh
King Saud University
Sayed-Ahmed, Mohamed M.
Saudi Arabia, Riyadh
King Saud University
Statistics
Citations: 102
Authors: 8
Affiliations: 1
Identifiers
Doi:
10.3748/wjg.15.1373
ISSN:
10079327
Research Areas
Cancer
Environmental
Study Design
Randomised Control Trial
Participants Gender
Male