Effects of zinc on hepatic antioxidant systems and the mRNA expression levels assayed by cDNA microarrays in rats.
BACKGROUND
This study evaluated effects of zinc on the hepatic lipid peroxidation, antioxidant components and mRNA expression levels in rats.


METHODS
Three diets with different Zn levels including Zn adequacy (ZA; 34.50 mg/kg, control), Zn deficiency (ZD; 3.30 mg/kg), and Zn overdose (ZO; 345.45 mg/kg) were fed to rats for 6 weeks. The mRNA expression levels were analyzed by cDNA microarrays.


RESULTS
The body weight of rats fed the ZD diet was less (p < 0.01) than that of rats fed the ZA diet. Zn overdose elevated body weight, but the increase was not detected (p > 0.05) at week 6. Although copper and iron status in serum were declined (p < 0.01), those in liver were not affected (p > 0.05) by the high intake of zinc. The glutathione peroxidase (GPx) and glutathione (GSH) remained unchanged (p > 0.05) by zinc treatment. Rats fed the ZD diet showed reductions(p < 0.01) in the Cu-Zn superoxide dismutase (Cu-Zn SOD) and catalase (CAT) activity, and increases (p < 0.01) in the malondialdehyde and hydrogen peroxide (H(2)O(2)) contents. Rats fed the ZO diet particularly had higher Cu-Zn SOD (p < 0.01) activity. The mRNA expression levels of SOD were upregulated in the ZO group, and CAT was downregulated in the ZD group, while no changes in GPx mRNA levels were found after zinc treatment.


CONCLUSIONS
The study suggested that zinc deficiency largely decreased body weight; zinc overdose, however, moderately stimulated growth in the early growing phase of rats. High dietary zinc did not compete with liver copper and iron status. Although Zn deficiency impaired antioxidant functions, zinc overdose hardly enhanced the antioxidant systems of animals.
Jing
Ming-Yan
MY
The Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Science, Zhejiang University, Hangzhou, PR China.
Sun
Jian-Yi
JY
Zi
Nai-Tao
NT
Sun
Wei
W
Qian
Li-Chun
LC
Weng
Xiao-Yan
XY
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D003300:Copper / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D007501:Iron / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis / Q000379:methods; D010084:Oxidation-Reduction; D012333:RNA, Messenger / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D015032:Zinc / Q000172:deficiency* / Q000494:pharmacology*
D000975:Antioxidants; D012333:RNA, Messenger; D008315:Malondialdehyde; D003300:Copper; D006861:Hydrogen Peroxide; D007501:Iron; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; D015032:Zinc