Effects of Selenium Deficiency on Gene Expression

Cells grown or maintained in selenium deficient media do not become spontaneously malignant, they still require a carcinogenic stimulus, which may be chemical, physical, viral or genetic. However, an insufficient supply of selenium evidently results in adaptive changes facilitating the malignant transformation of cells. The extent of these changes has recently been elucidated through a study (39) with cells from the intestine of mice. When these cells were grown under conditions of selenium deficiency, as many as 44 of their genes were up-regulated, among them genes associated with DNA repair and the protection against oxidative stress and genes controlling cell cycle. In addition, at least 24 genes were down-regulated, those involved with selenoprotein synthesis, the synthesis of enzymes involved in detoxification (cytochrome P450, GSH S-transferase, epoxide hy-drolase) as well as the synthesis of enzymes regulating lipid transport, angiogenesis, cell adhesion, cell cycle, and cell growth. All these changes point to diminished resistance to carcinogenic stress factors. The loss of cell cycle control alone, for example, may increase the error rate during DNA replication and prevent DNA repair. The down-regulation of the detoxifying enzymes may prevent carcinogens to be metabolized.

Mechanisms of Anticarcinogenic Action 173

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