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Intestinal inflammation in rats induces metallothionein in colonic submucosa.

Al-Gindan Y, Shawarby M, Noto A, Taylor CG - J Clin Biochem Nutr (2009)

Bottom Line: Serum zinc concentrations were attenuated in the DSS-challenged ZT and ZS groups suggesting that zinc was being utilized in some capacity in response to inflammation.DSS-challenge induced MT immunostaining in the colonic submucosa, however, MT was not associated with histological improvements in the present study.The site-specific MT induction in colonic submucosa during intestinal inflammation requires further clarification as a component of the host defense.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, MB R3T 2N2, Canada.

ABSTRACT
The aim of the current study was to determine if induction of metallothionein (MT) via acute or chronic dietary zinc supplementation attenuates intestinal inflammation, and to investigate the relationship with site-specific intestinal MT determined by immunolocalization. Growing rats were assigned to zinc-deficient (ZD), acute zinc-treated (ZT), pair-fed, control or chronic Zn-supplemented (ZS) groups. Half the rats in each dietary group received 5% dextran sulphate sodium (DSS) in their drinking water for 4 days. DSS treatment produced acute intestinal inflammation in the colon only, however, dietary zinc deficiency, acute zinc treatment or chronic zinc supplementation did not alter the severity of ulceration. Serum zinc concentrations were attenuated in the DSS-challenged ZT and ZS groups suggesting that zinc was being utilized in some capacity in response to inflammation. DSS-challenge induced MT immunostaining in the colonic submucosa, however, MT was not associated with histological improvements in the present study. The site-specific MT induction in colonic submucosa during intestinal inflammation requires further clarification as a component of the host defense.

No MeSH data available.


Related in: MedlinePlus

Colonic metallothionein localization. Metallothionein staining was weak in the submucosa of the ZD+ group (A), absent in the ZD− group (B); all other DSS+ groups had staining in the submucosa and crypts (C, E, G, I) while the DSS− groups had staining only in the crypts (D, F, H, J) as indicated by scoring: (−−) none to very weak, (+) mild, (++) moderate, (+++) high of submocosa and crypts. − = no dextran sulfate sodium challenge, + = 5% dextran sulfate sodium challenge; ZD = zinc deficient (3 mg/kg zinc), PF = pair fed (30 mg/kg zinc) to match energy intake of ZD group, ZT = zinc deficient (3 mg/kg zinc) and repleted (300 mg/kg zinc), C = control (30 mg/kg zinc), ZS = zinc supplemented (300 mg/kg zinc).
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Figure 5: Colonic metallothionein localization. Metallothionein staining was weak in the submucosa of the ZD+ group (A), absent in the ZD− group (B); all other DSS+ groups had staining in the submucosa and crypts (C, E, G, I) while the DSS− groups had staining only in the crypts (D, F, H, J) as indicated by scoring: (−−) none to very weak, (+) mild, (++) moderate, (+++) high of submocosa and crypts. − = no dextran sulfate sodium challenge, + = 5% dextran sulfate sodium challenge; ZD = zinc deficient (3 mg/kg zinc), PF = pair fed (30 mg/kg zinc) to match energy intake of ZD group, ZT = zinc deficient (3 mg/kg zinc) and repleted (300 mg/kg zinc), C = control (30 mg/kg zinc), ZS = zinc supplemented (300 mg/kg zinc).

Mentions: MT immunostaining was nondetectable in the unchallenged ZD group whereas it was very weak in the submucosa of the DSS-challenged ZD rats (Fig. 5A, B). All other DSS-challenged rats had MT staining in the crypts and submucosa (Fig. 5C, E, G, I), while the non-challenged rats had MT immunostaining only in the crypts (Fig. 5D, F, H, J). The strongest crypt staining was seen in the unchallenged ZT rats (Fig. 5F) and the unchallenged ZS rats (Fig. 5J). There was strong submucosal staining in the DSS-challenged PF, ZT, C and ZS rats (Fig. 5C, E, G, I, respectively).


Intestinal inflammation in rats induces metallothionein in colonic submucosa.

Al-Gindan Y, Shawarby M, Noto A, Taylor CG - J Clin Biochem Nutr (2009)

Colonic metallothionein localization. Metallothionein staining was weak in the submucosa of the ZD+ group (A), absent in the ZD− group (B); all other DSS+ groups had staining in the submucosa and crypts (C, E, G, I) while the DSS− groups had staining only in the crypts (D, F, H, J) as indicated by scoring: (−−) none to very weak, (+) mild, (++) moderate, (+++) high of submocosa and crypts. − = no dextran sulfate sodium challenge, + = 5% dextran sulfate sodium challenge; ZD = zinc deficient (3 mg/kg zinc), PF = pair fed (30 mg/kg zinc) to match energy intake of ZD group, ZT = zinc deficient (3 mg/kg zinc) and repleted (300 mg/kg zinc), C = control (30 mg/kg zinc), ZS = zinc supplemented (300 mg/kg zinc).
© Copyright Policy - open-access
Related In: Results  -  Collection

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Figure 5: Colonic metallothionein localization. Metallothionein staining was weak in the submucosa of the ZD+ group (A), absent in the ZD− group (B); all other DSS+ groups had staining in the submucosa and crypts (C, E, G, I) while the DSS− groups had staining only in the crypts (D, F, H, J) as indicated by scoring: (−−) none to very weak, (+) mild, (++) moderate, (+++) high of submocosa and crypts. − = no dextran sulfate sodium challenge, + = 5% dextran sulfate sodium challenge; ZD = zinc deficient (3 mg/kg zinc), PF = pair fed (30 mg/kg zinc) to match energy intake of ZD group, ZT = zinc deficient (3 mg/kg zinc) and repleted (300 mg/kg zinc), C = control (30 mg/kg zinc), ZS = zinc supplemented (300 mg/kg zinc).
Mentions: MT immunostaining was nondetectable in the unchallenged ZD group whereas it was very weak in the submucosa of the DSS-challenged ZD rats (Fig. 5A, B). All other DSS-challenged rats had MT staining in the crypts and submucosa (Fig. 5C, E, G, I), while the non-challenged rats had MT immunostaining only in the crypts (Fig. 5D, F, H, J). The strongest crypt staining was seen in the unchallenged ZT rats (Fig. 5F) and the unchallenged ZS rats (Fig. 5J). There was strong submucosal staining in the DSS-challenged PF, ZT, C and ZS rats (Fig. 5C, E, G, I, respectively).

Bottom Line: Serum zinc concentrations were attenuated in the DSS-challenged ZT and ZS groups suggesting that zinc was being utilized in some capacity in response to inflammation.DSS-challenge induced MT immunostaining in the colonic submucosa, however, MT was not associated with histological improvements in the present study.The site-specific MT induction in colonic submucosa during intestinal inflammation requires further clarification as a component of the host defense.

View Article: PubMed Central - PubMed

Affiliation: Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, MB R3T 2N2, Canada.

ABSTRACT
The aim of the current study was to determine if induction of metallothionein (MT) via acute or chronic dietary zinc supplementation attenuates intestinal inflammation, and to investigate the relationship with site-specific intestinal MT determined by immunolocalization. Growing rats were assigned to zinc-deficient (ZD), acute zinc-treated (ZT), pair-fed, control or chronic Zn-supplemented (ZS) groups. Half the rats in each dietary group received 5% dextran sulphate sodium (DSS) in their drinking water for 4 days. DSS treatment produced acute intestinal inflammation in the colon only, however, dietary zinc deficiency, acute zinc treatment or chronic zinc supplementation did not alter the severity of ulceration. Serum zinc concentrations were attenuated in the DSS-challenged ZT and ZS groups suggesting that zinc was being utilized in some capacity in response to inflammation. DSS-challenge induced MT immunostaining in the colonic submucosa, however, MT was not associated with histological improvements in the present study. The site-specific MT induction in colonic submucosa during intestinal inflammation requires further clarification as a component of the host defense.

No MeSH data available.


Related in: MedlinePlus