El-Gendy, A. (2011). Amelioration of aluminium - intake oxidative stress by some antioxidants in male albino rats. The Egyptian Journal of Hospital Medicine, 45(1), 536-546. doi: 10.21608/ejhm.2011.16384
Ahkam M. El-Gendy. "Amelioration of aluminium - intake oxidative stress by some antioxidants in male albino rats". The Egyptian Journal of Hospital Medicine, 45, 1, 2011, 536-546. doi: 10.21608/ejhm.2011.16384
El-Gendy, A. (2011). 'Amelioration of aluminium - intake oxidative stress by some antioxidants in male albino rats', The Egyptian Journal of Hospital Medicine, 45(1), pp. 536-546. doi: 10.21608/ejhm.2011.16384
El-Gendy, A. Amelioration of aluminium - intake oxidative stress by some antioxidants in male albino rats. The Egyptian Journal of Hospital Medicine, 2011; 45(1): 536-546. doi: 10.21608/ejhm.2011.16384
Amelioration of aluminium - intake oxidative stress by some antioxidants in male albino rats
Aluminum is potentially toxic to humans. The Agency for Toxics Substances and Disease Registry (ATSDR) reported that aluminum accumulates mainly in the bone, liver, testes, kidneys and brain. The goal of the present study was to assess in rats the pro-oxidant effects induced by Al3+ exposure, as well as the protective role of exogenous melatonin (M), vitamin E (vit. E) or N-acetylcystiene (NAC). The effect of aluminium (Al) alone or combined with antioxidants (M), (vit. E) or (NAC) on some physiological parameters and antioxidants in male albino rats were studied.
Material and methods:
The animals were assigned to 5 groups: control (group I); Al3+–intake (53.5 mg AlCl3/litre drinking water , group II) ; 5 mg melatonin/kg b.wt. plus AlCl3 (group III); , or vitamin E(100 mg/kg b.w.) plus AlCl3 (group IV)or 100mg N-acetylcystien plus AlCl3 (group V). Rats were orally administered their respective doses daily for 30 days. At the end of the treatment period, blood was obtained. Thereafter, brain, liver, kidney and testes were removed. These tissues were processed to examine oxidative stress markers: reduced glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (GSHpx) and lipid peroxidation end products {malondialdhyde(MDA) + 4- hydroxynonenal (4- HNE)}. Samples of these tissues were also used to determine Al3+ concentrations.
Results :
In Al- toxicated group ,serum glucose and total cholesterol levels, liver enzyme activities (ASAT and ALAT), as well as, lipid peroxidation end products {malondialdhyde (MDA) + 4- hydroxynonenal (4- HNE)} were elevated significantly in the brain , liver ,kidney and testes tissues when compared with control group. On the other hand, serum triglycerides and tissue (liver, kidney and testes) intracellular antioxidants glutathione (GSH) and superoxide dismutase (SOD) and liver glutathione peroxidase (GSHpx) activity decreased significantly. Brain GSH also decreased but SOD showed no significant changes. Melatonin, vit. E and NAC improved the levels of the different changed parameters when combined with Al. The most improved correction was recorded when Al3+ combined with vit. E followed by M ,then NAC. Serum Al3+ levels were increased in Al3+ treated group as well as groups exposed to Al3+ combined with vit. E, M or NAC when compared with control group. Al3+ could not be detected in tissues by atomic spectrophotometer (aluminium metal concentrations were below the limit of detection by AAS).
Conclusion:
The results show that Al3+ exposure promotes oxidative stress in different tissues while melatonin, vitamin E and N-acetylcystiene exert antioxidant actions in Al3+-treated animals. The protective effects of these antioxidants against cellular damage caused by Al3+-induced oxidative stress, together with its low toxicity, make them worthy of investigation as potential supplements to be included in the treatment of neurological disorders in which the oxidative effects must be minimized as well as protection against liver, kidney and testes damage by Al- exposure.
Dietary vitamin E supplementation may offer further protection.
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