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Hepatic Irradiation

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5.3.2 Markers of radiation-induced hepatic injury
Of the liver enzymes that showed elevations in their serum concentrations following irradiation in the current study, only the early increase in the AST level was significant (Fig. 9). ALT is also a marker of hepatic damage, and it is found exclusively in the cytoplasm of cells. In contrast, AST is present in the cytoplasm, which comprises 20% of its total activity, and in the mitochondria, which comprises 80% of its total activity (Rej 1989). While the recruited granulocytes and the gamma irradiation could damage some periportal hepatocytes, irradiation treatment may have a more damaging effect on the numerous large mitochondria that reside within the hepatocytes, which would lead to a greater
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10). Interestingly, these granulocytes were only detectable in the portal area between and around the Thy-1+ LMFs (Fig. 14), and they were not present along the sinusoids or around the central vein. The levels of ED1+ or ED2+ mononuclear phagocytes did not increase at any time after irradiation (Fig. 12).
In classical inflammation, macrophages follow the neutrophils to the site of the injury. The absence of mononuclear phagocytes at the site of the injury following irradiation in the present study could be associated with irradiation-induced structural modifications within these cells that could weaken the defence response. It is possible that mononuclear phagocytes lose their normal defence functions after irradiation and that they become unable to increase in number. Furthermore, the post-irradiation releases of the inflammatory mediators that recruit mononuclear phagocytes may not reach the threshold levels that are required to mobilise the macrophages, and inflammatory mediators regulate leukocyte production in the bone marrow. Irradiation may also alter the levels of gene expression associated with the inflammatory mediators and adhesion molecules that are required for macrophage transmigration, thereby preventing its occurrence. A previous study that
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2003). However, endothelial cells may play a minor role in the transmigration of the inflammatory cells because irradiating these cells in vitro did not upregulate chemokine gene expression (Gaugler et al. 1998). This may also support the notion that the mesenchymal cells of the sinusoidal wall, that is, the hepatic stellate cells, differ from the Thy-1+ mesenchymal cells in the portal vessels and in the portal area (Dudas et al.
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