This study aimed to investigate the potential effects of melatonin on aluminium-induced toxicity in a rat model using a set of biochemical, inflammatory, oxidant, lipid profile criteria and hepatic integrity (verified by hematoxylin-eosin staining). The results indicated that AlCl3 administration during 60 days (100 mg/kg b.w.) significantly increased the activities of transaminases AST and ALT by 46% (p < 0.001) and 21% (p < 0.01), lactate dehydrogenase (LDH) by 30% (p < 0.001), the levels of bilirubin by 85% (p < 0.001), total cholesterol by 115% (p < 0.001), triglycerides by 130% (p < 0.001), LDL-cholesterol by 413% (p < 0.001), oxidized LDL (oxLDL) by 51% (p < 0.01) and apolipoprotein B100 (apoB100) by 63% (p < 0.001), as compared to controls. The inflammatory markers (TNF-α, IL-2, and IL-6) were significantly increased (p < 0.001), associated to higher lipid peroxidation (TBARS) level. Also, both plasma HDL-cholesterol level and hepatic LDL receptors (p < 0.01) expression and antioxidant protein (SOD, CAT, and GPx) activities are decreased. Those physiological disturbances were, however, noted to alleviate following the co-administration of melatonin (10 mg/kg b.w.). Overall, the present study is the first to provide evidence on the anti-inflammatory, anti-oxidant, anti-lipidic and, hence, therapeutic effects of melatonin with regard to the control and prevention of aluminium-intoxication.

Download full-text PDF

Source
http://dx.doi.org/10.4149/gpb_2015028DOI Listing

Publication Analysis

Top Keywords

melatonin aluminium-induced
8
aluminium-induced toxicity
8
effects melatonin
8
0001
8
pleiotropic protective
4
protective roles
4
melatonin
4
roles melatonin
4
toxicity rats
4
rats study
4

Similar Publications

This study aimed to investigate the potential effects of melatonin on aluminium-induced toxicity in a rat model using a set of biochemical, inflammatory, oxidant, lipid profile criteria and hepatic integrity (verified by hematoxylin-eosin staining). The results indicated that AlCl3 administration during 60 days (100 mg/kg b.w.

View Article and Find Full Text PDF

The protective properties of melatonin against aluminium-induced neuronal injury.

Int J Exp Pathol

June 2015

Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt.

Aluminium (Al) toxicity is closely linked to the pathogenesis of Alzheimer's disease (AD). This experimental study investigated the neuroprotective effect of melatonin (Mel; 10 mg/kg bwt) on aluminium chloride (AlCl3 ; 34 mg/kg bwt) induced neurotoxicity and oxidative stress in rats. Adult male albino Wistar rats were injected with AlCl3 for 7 days.

View Article and Find Full Text PDF

Effects of melatonin on aluminium-induced neurobehavioral and neurochemical changes in aging rats.

Food Chem Toxicol

August 2014

Laboratory of Animal Ecophysiologie, Faculty of Science of Sfax, 3018 Sfax, Tunisia.

This study aimed to investigate the potential protective effects of melatonin (Mel) against aluminium-induced neurodegenerative changes in aging Wistar rats (24-28months old). Herein, aluminium chloride (AlCl3) (50mg/kg BW/day) was administered by gavage, and melatonin (Mel) was co-administered to a group of Al-treated rats by an intra-peritoneal injection at a daily dose of 10mg/kg BW for four months. The findings revealed that aluminium administration induced a significant decrease in body weight associated with marked mortality for the old group of rats, which was more pronounced in old Al-treated rats.

View Article and Find Full Text PDF

The serum concentrations of aluminum, a metal potentially involved in the pathogenesis of Alzheimer's disease, increase with age. Also, intense and prolonged exposure to aluminum may result in dementia. Melatonin and pinoline are two well known antioxidants that efficiently reduce lipid peroxidation due to oxidative stress.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!