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 new research article 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.
Journal 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 http://www.wjgnet.com/1007-9327/14/76.asp
Materials provided by World Journal of Gastroenterology. Note: Content may be edited for style and length.
Cite This Page: