Effect of Vitamin E Supplementation on mRNA Expression of Superoxide Dismutase and Interleukin-2 in Arsenic Exposed Goat Leukocytes
2. Zero hunger
0303 health sciences
Superoxide Dismutase
Goats
Antioxidants
Hazardous Substances
Arsenic
03 medical and health sciences
Dietary Supplements
Leukocytes
Animals
Interleukin-2
Vitamin E
RNA, Messenger
DOI:
10.1007/s00128-012-0825-2
Publication Date:
2012-10-01T01:59:12Z
AUTHORS (8)
ABSTRACT
The aim of this study was to quantify the expression level of genes involved in antioxidant defenses during inorganic arsenic (iAs) exposure in the blood of goats and to evaluate the regulative activity on these genes of antioxidant vitamin E in the diet. Twenty-four crossbred lactating goats (Alpine × Beetal) were distributed randomly into four equal groups (Control, T(1), T(2) and T(3)) of six in each, on the basis of average body weight (36.10 ± 0.11 kg) and milk yield (1.61 ± 0.004 kg/day). The animals in T(1), T(2) and T(3) were given 50 mg/kg dry matter arsenic daily, while in T(2) and T(3), vitamin E @100 IU and 150 IU/kg dry matter, respectively, was also supplemented additionally for the period of 12 months. Blood was sampled at 0 day then at 3 months interval and analyzed for the expression level of superoxide dismutase (Cu/Zn SOD) and interleukin-2 (IL-2) using real-time PCR technique. Initially there was no difference (p > 0.05) in relative expression of the two genes. But, at 3 months, relative expression of Cu/Zn SOD increased (p < 0.05) in T(1) groups then, at 6 and 9 months expression was decreased (p < 0.05) in all the iAs treated groups whereas at 12 months, vitamin E supplementation increased (p < 0.05) the expression which is comparable to control groups. IL-2 mRNA expression was decreased (p < 0.05) at 6 months in all iAs treated groups, at 9 months there was decline trend but not significantly different whereas at 12 months decline trend was less (p < 0.05) in vitamin E supplemented groups. The result suggests that vitamin E may have a controlling effect on oxidative stress through modulation of SOD and IL-2 expression.
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