Abstract
The current literature data on the metabolic effects of ethionine in mammalian cells, as well as the results of our own research are summarized in the present paper. Ethionine is an S-ethyl analogue of methionine that prevents the methylation of macromolecules (DNA, RNA, proteins and lipids). It has carcinogenic properties and inhibits the growth of certain microorganisms in the gastrointestinal tract. Competing with methionine at the stage of translation, ethionine reduces the specific activity of the protein. The extreme toxicity of ethionine is explained by the need for methionine in many biosynthetic and regulatory processes. At the organ level (in vivo), the intake of ethionine causes fatty degeneration of the liver (“nutmeg” liver) and acute pancreatitis; it also induces the development of liver carcinoma. Ethionine has a negative effect on the proliferation of lymphocytes, it completely suppresses DNA synthesis in lymphocytes stimulated by phytohemagglutinin or concanavalin A. This methionine analog inhibits tRNA methylation and prevents the increase in the activity of histone-modifying enzymes caused by the mitogen. The cessation of ethionine intake leads to a fast synchronous wave of DNA synthesis, an increase in the rate of RNA methylation, as well as a rise in the activity of histone-modifying enzymes. Given the multifaceted effect of ethionine on metabolic processes, it can be assumed that its potential as an antimetabolite of methionine is underestimated and further research is needed in this direction.
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