Enterocyte viability and mitochondrial function after graded intestinal ischemia and reperfusion in rats

Madesh, Muniswamy ; Bhaskar, Lakshmi ; Balasubramanian, K. A. (1997) Enterocyte viability and mitochondrial function after graded intestinal ischemia and reperfusion in rats Molecular and Cellular Biochemistry, 167 (1-2). pp. 81-87. ISSN 0300-8177

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Official URL: http://www.springerlink.com/content/jx3260k621120k...

Related URL: http://dx.doi.org/10.1023/A:1006871622049


Ischemia/reperfusion of the small intestine can lead to metabolic and structural alterations in the mucosa. Cellular dysfunction occurs when mitochondrial metabolism is compromised, which may ultimately lead to impaired organ function. The aims of this study were to assess the suppression of cellular and mitochondrial oxidative metabolism and involvement of mitochondria in the ischemia/reperfusion injury. The mitochondria were prepared from isolated enterocytes obtained from the small intestine of anesthetized adult rats following different time periods of ischemia and ischemia followed by 5 min reperfusion. Cellular and mitochondrial function were assessed using MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) reduction assay. Ischemia of increasing time periods caused a progressive decrease in cellular and mitochondrial MTT reduction in enterocytes and reperfusion showed further decrease of MTT formazan formation. Inclusion of 1 mM succinate, as respiratory subs trate, showed reversal of suppression of mitochondrial function in 30-60 min ischemia whereas 90 min ischemia or short time period ischemia followed by 5 min reperfusion indicated an irreversible damage to mitochondria. This study indicated that mitochondria are a sensitive target of damage due to oxygen deficiency and possibly due to sudden burst of oxygen free radicals. Mitochondria can withstand short periods of ischemia whereas long duration ischemia or reperfusion results in irreversible damage to mitochondrial function.

Item Type:Article
Source:Copyright of this article belongs to Springer-Verlag.
Keywords:Ischemia/Reperfusion; MTT Reduction; Enterocyte Viability; Mitochondrial Dysfunction
ID Code:1426
Deposited On:04 Oct 2010 11:19
Last Modified:14 May 2011 05:09

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