الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
 |  | from | 15 |  |  |
| | | from | 15 | | |
Abstract
Many previous studies demonstrated the toxic effect of cadmium chloride on the liver, so at this study L- carnitine was used to mitigate the harmful effect of cadmium chloride through normalization of biochemical parameters and histopathological changes induced by it. This protective role of L-carnitine comes from the fact that it is a well-known potent antioxidant. In This study the histological, histochemical, immunohistochemical and physiological methods were used to demonstrate the action of L-carnitine.
1. Histopathological observations
In the liver of rats supplemented with cadmium chloride 0.88 mg/kg for 14 days revealed different degree of cell degeneration, focal necrosis of hepatocytes, dilatation and congestion of portal vein. Hepatic cell damage was such as pyknosis and karyohexsis of nuclei, narrowed of the sinusoids, hypactivity of Kupffer cells. Also lymphocytic infiltration in the portal and periportal areas, and hydropic degeneration were found.
Rats exposed to the combined administration of L-carnitine before or after Cd treatment showed a mild degree of lesions when compared to the Cd treated group. Rats treated with L-carnitine alone showed no changes take place and kept the organ almost similar to that of control.
2. The Histochemical observations
1. Total protein
Liver of rats supplemented with L-carnitine for 14 days revealed the total proteins appear as intense deep blue inclusions in the cytoplasm of the hepatic cells. Cd-treated rats showed obvious change in the protein content
of hepatocytes cells and lost most of their protein content, the cytoplasm of degenerated hepatocytes was slightly stained with blue color due to a severe depletion of the protein content. Examination of liver sections of L-carnitine and pre or post cadmium chloride treated rats showed an increase in protein content as compared to cadmium chloride treated animals.
2. Deoxyribonucleic acid (DNA)
Liver section of L-carnitine treated rat showing no changes in the DNA content. Examination of liver section of rat received CdCl2 for 14 days revealed most of the nuclei were lightly stained; the DNA-contents were reduced in the nucleoplasm of the hepatic cells. The groups contained cadmium chloride treated rat and pre or post-treated with L-carnitine showed that DNA contents were moderately stained in the nuclei. The nuclei restored their DNA contents and appeared more or less as in the control.
3. The Immunohistochemistry examination COX2
Liver sections of control and L-carnitine treated rat showed no expression of COX2. Liver section of CdCl2 treated rats showing positive immunoreactivity of COX2, as indicated by intense brown color reaction as compared to the control group. Liver sections of rat treated with CdCl2 and pre-treated or post- treated with L-carnitine showing a significant decrease in COX2 immunoreactivity as indicated by moderate intensity of brown color as compared to cadmium chloride treated group.
4. Biochemical results
a) Aspartate transaminase (ALT & AST)
Significant increases (P < 0.05) in asparate transaminase (AST) and serum alanine transferase (ALT) found in cadmium chloride treated animals as compared with control one. Administration with L-carnitine and with CdCl2 (pre or post-treated) exhibited significant decrease (P < 0.01) in ALT & AST as compared with the CdCl2 treated animals.
b) Alkaline phosphatase (AL Ph)
Exposed rats to cadmium chloride showed significant increase (P < 0.05) in AL Ph as compared with the control. On the other hand supplemented rats with CdCl2 and L-carnitine showed significant decrease (P < 0.01) in AL Ph when compared with CdCl2 treated groups.
VII. Conclusion
It was found that L-carnitine has a significant hepatoprotective effect against cadmium chloride-induced liver damage. L-carnitine can attenuate cadmium chloride-induced oxidative stress and improve liver functions. So if relevant in humans, this finding may be of a major importance, introducing for the first time a safe, inexpensive and feasible method for attenuation of cadmium chloride-induced hepatotoxicity.