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Effects of mild zinc deficiency, plus or minus an acute-phase response, on galactosamine-induced hepatitis in rats

Published online by Cambridge University Press:  09 March 2007

Susan E. Parsons  and
Robert A. Disilvestro
Susan E. Parsons
Affiliation:
Human Nutrition and Food Management, Ohio State University, 265 Campbell Hall, 1787 Neil Avenue, Columbus, OH 43210, USA
Robert A. Disilvestro
Affiliation:
Human Nutrition and Food Management, Ohio State University, 265 Campbell Hall, 1787 Neil Avenue, Columbus, OH 43210, USA
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Abstract

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Zn deficiency is hypothesized to produce poor resistance to injury involving oxidative stress. This could occur by impairing Zn antioxidant function(s) or by indirectly limiting adaptive protective mechanisms such as a rise in acute-phase proteins. The present study examined rats fed diets adequate or moderately low in Zn (4 or 25 μg/g diet) for 9 d. The lower intake produced a mild Zn deficiency based on body weight, plasma Zn and plasma alkaline phosphatase (EC 3.1.3.1) activity. Galactosamine injection, an oxidative stress, produced much more liver injury in the mildly Zn-deficient rats. However, injury was strongly inhibited in rats from each dietary group by an acute-phase response due to turpentine-induced leg inflammation. Mild Zn deficiency did not prevent a rise in levels of the acute-phase protein caeruloplasmin (EC 1.16.3.1), but did limit the usual inflammation-induced rise in hepatic levels of metallothionein, a Zn protein with possible antioxidant function. In conclusion, high degrees of galactosamine-induced hepatitis were associated with mild Zn deficiency, but the liver injury was blocked by prior stimulation of an acute-phase response, regardless of Zn status.

Keywords

ZincGalactosamine-induced hepatitisMetallothionein
Type
Zinc deficiency and the acute phase response
Information
British Journal of Nutrition , Volume 72 , Issue 4 , October 1994 , pp. 611 - 618
Copyright
Copyright © The Nutrition Society 1994

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