Thioredoxin reductase activity is decreased by selenium deficiency

Area of Science:

• Biochemistry
• Nutritional Science
• Toxicology

Background:

• Animal thioredoxin reductase (TrxR) is a crucial selenoprotein involved in cellular redox homeostasis.
• Selenium is an essential trace element vital for the function of various selenoenzymes, including TrxR.

Purpose of the Study:

• To investigate the impact of selenium deficiency on thioredoxin reductase activity in different rat organs.
• To compare the sensitivity of TrxR activity in liver, kidney, and brain to selenium nutritional status.

Main Methods:

• Rats were fed selenium-deficient or control diets for 14 weeks post-weaning.
• Thioredoxin reductase activity was measured in liver, kidney, and brain homogenates.
• Effects of gold inhibition and selenium repletion on TrxR activity were assessed.

Main Results:

• Selenium deficiency markedly decreased TrxR activity in the liver (to 4.5% of control) and kidney (to 11% of control).
• Brain TrxR activity remained unaffected by the induced selenium deficiency.
• Gold inhibited liver TrxR activity, consistent with its known effects on selenoenzymes.
• Selenium repletion restored TrxR activity in the liver more rapidly than glutathione peroxidase but slower than selenoprotein P.

Conclusions:

• Liver and kidney thioredoxin reductase activity are highly sensitive to selenium nutritional status.
• Brain thioredoxin reductase exhibits lower sensitivity to selenium deficiency compared to liver and kidney.
• These findings underscore the organ-specific impact of selenium levels on selenoenzyme function.