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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Hagar, Hanan Al Malki, Waleed |
| Description | Author Affiliation: Hagar H ( Department of physiology and Pharmacology, College of Medicine, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia. Electronic address: hananhhagar@yahoo.com.); Al Malki W ( Department of Pharmacology, College of Pharmacy Umm Al-Qura University, Makkah, Saudi Arabia.) |
| Abstract | Cadmium (Cd) is an environmental and industrial pollutant that can induce a broad spectrum of toxicological effects that affect various organs in humans and experimental animals. This study aims to investigate the effect of betaine supplementation on cadmium-induced oxidative impairment in rat kidney. The animals were divided into four groups (n=10 per group): control, cadmium, betaine and betaine+cadmium (1) saline control group; (2) cadmium group in which cadmium chloride (CdCl2) was given orally at a daily dose of 5 mg/kg body weight for four weeks; (3) betaine group, in which betaine was given to rats at a dose of 250 mg/kg/day, orally via gavage for six weeks; (4) cadmium+betaine group in which betaine was given at a dose of 250 mg/kg/day, orally via gavage for two weeks prior to cadmium administration and concurrently during cadmium administration for four weeks. Cadmium nephrotoxicity was indicated by elevated blood urea nitrogen (BUN) and serum creatinine levels. Kidneys from cadmium-treated rats showed an increase in lipid peroxidation measured as thiobarbituric acid-reactive substances (TBARS) concentration and reductions in total antioxidant status (TAS), reduced glutathione (GSH) content, glutathione peroxidase (GSH-Px) activity, superoxide dismutase concentration (SOD) and catalase activity. Caspase-3 activity, a marker of DNA damage was also elevated in renal tissues of cadmium-treated rats. Pre-treatment of rats with betaine substantially attenuated the increase in BUN and serum creatinine levels. Betaine also inhibited the increase in TBARS concentration and reversed the cadmium-induced depletion in total antioxidant status, GSH, GSH-Px, SOD and catalase concentrations in renal tissues. Renal caspase-3 activity was also reduced with betaine supplementation. These data emphasize the importance of oxidative stress and caspase signaling cascade in cadmium nephrotoxicity and suggest that betaine pretreatment reduces severity of cadmium nephrotoxicity probably via antioxidant action and suppression of apoptosis. |
| File Format | HTM / HTML |
| ISSN | 13826689 |
| Issue Number | 2 |
| Volume Number | 37 |
| e-ISSN | 18727077 |
| Journal | Environmental Toxicology and Pharmacology |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2014-03-01 |
| Publisher Place | Netherlands |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Environmental Health Discipline Pharmacology Betaine Therapeutic Use Cadmium Toxicity Environmental Pollutants Kidney Drug Effects Protective Agents Animals Pharmacology Cadmium Poisoning Drug Therapy Metabolism Caspase 3 Glutathione Glutathione Peroxidase Male Oxidative Stress Rats, Wistar Superoxide Dismutase Thiobarbituric Acid Reactive Substances Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Health, Toxicology and Mutagenesis Medicine Toxicology Pharmacology |
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