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.
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The proteasome is important as it maintains the equilibrium of the cell, said Dr Delneri. When this equilibrium is lost it can result in a number of diseases, including cancer, diabetes, Huntingdon's, Alzheimer's and Parkinson's.
For example, in rapidly-growing cancerous cells the high proteasome activity renders the tumour cells immortal, so drugs that block or inhibit the proteasome's actions are currently used as therapeutic compounds.
Our study shows that reduced proteasome activity could be either advantageous or damaging to the cell depending on the nutrients available to it in the surrounding environment.
The findings suggest that, ideally, when therapeutic drugs are administered to alter the proteasome activity, the environment “ governed by the type of tissue or a person's diet and lifestyle “ should be taken into consideration to assure the correct beneficial effect.
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