| ORIGINAL ARTICLE |
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| Year : 2020 | Volume
: 5
| Issue : 2 | Page : 37-47 |
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Doxycycline: An antibiotic with brain protective function in vanadium-intoxicated rats
Negia Abdullah Emtawel Mohamed1, Ezeddin Salem Gassar2, Sara A Abdulla1, Mustafa Mohamed Elfakhri1, Ayyub Patel3, Syed Saleem Haider3
1 Department of Biochemistry, Faculty of Medicine, Benghazi University, Benghazi, Libya
2 Department of Physiology, Faculty of Medicine, Benghazi University, Benghazi, Libya
3 Department of Clinical Biochemistry, College of Medicine, King Khalid University, Abha, Saudi Arabia
Correspondence Address:
Syed Saleem Haider
Department of Clinical Biochemistry, College of Medicine, King Khalid University, P. O. Box 641, Abha 61321
Saudi Arabia
 Source of Support: None, Conflict of Interest: None  | 2 |
DOI: 10.4103/LIUJ.LIUJ_29_20
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Background: Exposure to vanadium exhibits deleterious neurotoxicity. Doxycycline is a potential antioxidant that prevents the progression of disease through inhibition of lipid peroxidation. Objectives: This research investigates the neuroprotective effects of doxycycline, in different rat brain areas in an animal model intoxicated with vanadium. Materials and Methods: Male Sprague-Dawley rats were equally divided into the following four groups: control group, doxycycline-treated group, vanadium-treated group, and concomitant doses of doxycycline plus vanadium-treated group, all given orally for 10 consecutive days. The animals were watched daily for any signs of neurological defects. They were sacrificed by decapitation 24 h after the last dose. Brain was removed rapidly and dissected into cerebral cortex, cerebellum, and brain stem. Biochemical studies including the concentrations of phospholipids, cholesterol, cerebrosides, glutathione (GSH), acetylcholinesterase (AChE) activity, gangliosides, ascorbic acid, calcium, and lipid peroxidation levels were determined. Results: The results revealed that vanadium produced significant reduction in body and absolute brain weight, with neurological function deficits. Vanadium significantly decreased the concentrations of phospholipids, cholesterol, cerebrosides, and GSH and inhibited AChE activity together with significant increase in gangliosides, ascorbic acid, calcium, and lipid peroxidation levels compared to saline controls. Animals which were given the combined treatment of vanadium and doxycycline regained weight and became normal. Moreover, doxycycline reversed the effect of vanadium on the metabolic variables and inhibited lipid peroxidation nearing to normal levels to that of saline controls. Conclusion: These findings demonstrated the antioxidant or chelating action of doxycycline against vanadium neurotoxicity and its therapeutic potential to avert neurodegenerative changes in different rat brain areas.
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