Cadmium comes from a wide variety of sources in the environment and from industry and is extremely toxic to humans. Environmental exposure can occur via the diet and drinking water. In chronic exposure, it also accumulates in the body, particularly in the kidneys and the liver. The liver acts as a detoxification organ. It filters the blood coming from the gastrointestinal tract and liver cells can be exposed to almost whole ingested and absorbed molecules and toxins at their highest concentrations through the portal vein. At present, there is no effective treatment for cadmium intoxication other than symptomatic treatment. Some chelating compounds are used for this purpose.
A research article published on January 7, 2008 in the World Journal of Gastroenterology (volume 14, issue 1) addresses this problem. An understanding of the processes that ensure self-protection against toxic substances is essential for the development and application of new therapeutic regimens. In research conducted in hepatocyte cell culture, cadmium exposure causes dose and time dependent damage in liver cells. Dr. Yazihan et al found cadmium intoxication stimulates secretion of midkine in a dose and time dependent manner. Midkine is mitogenic to cells. Midkine expression is found in the liver from early gestation. It is a heparin binding growth factor that regulates cell growth, survival, and differentiation. In this study it was found that exogenous midkine application induces hepatocyte proliferation. Midkine treatment prevented apoptosis, lactate dehydrogenase leakage and cytotoxicity caused by cadmium exposure in Hep3B cells. Midkine secretion might be one of the self defense mechanisms of the hepatocytes. The results of this study suggest a promising future therapy with midkine in cadmium induced hepatotoxicity. Midkine may also be beneficial to other hepatotoxic conditions.
6.1 Reference: Yazihan N, Ataoglu H, Akcil E, Yener B, Salman B, Aydin C. Midkine secretion protects Hep3B cells from cadmium induced cellular damage. World J Gastroenterol 2008; 14(1): 76-80
6.2 Correspondence to: Nuray Yazihan, MD, PhD, Molecular Biology Research and Development Unite, Faculty of Medicine, Ankara University, Morfoloji Binasi, Sihhiye, Ankara 06100, Turkey. firstname.lastname@example.org
Telephone: +90-312-3103010-372 Fax: +90-312-3106370
6.3 About World Journal of Gastroenterology
World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. The WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.
6.4 About The WJG Press
The WJG Press mainly publishes World Journal of Gastroenterology.
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