Selenous acid can also be made directly by oxidizing elemental selenium with nitric acid:

  
    
      
        
          3
          
          Se
          +
          4
          
          
            HNO
            
              3
            
            
              
            
          
          +
          
            H
            
              2
            
            
              
            
          
          O
          ⟶
          3
          
          
            H
            
              2
            
            
              
            
          
          
            SeO
            
              3
            
            
              
            
          
          +
          4
          
          NO
        
      
    
    {\displaystyle {\ce {3 Se + 4 HNO3 + H2O -> 3 H2SeO3 + 4 NO}}}
  Unlike sulfur, which forms a stable trioxide, selenium trioxide is thermodynamically unstable and decomposes to the dioxide above 185 °C:

  
    
      
        
          2
          
          
            SeO
            
              3
            
            
              
            
          
          ⟶
          2
          
          
            SeO
            
              2
            
            
              
            
          
          +
          
            O
            
              2
            
            
              
            
          
        
      
    
    {\displaystyle {\ce {2 SeO3 -> 2 SeO2 + O2}}}
   (ΔH = −54 kJ/mol)Selenium trioxide is produced in the laboratory by the reaction of anhydrous potassium selenate (K2SeO4) and sulfur trioxide (SO3).Salts of selenous acid are called selenites.
(Only the deiodinase iodotyrosine deiodinase, which works on the last breakdown products of thyroid hormone, does not use selenium. )Selenium may inhibit Hashimotos disease, in which the bodys own thyroid cells are attacked as foreign. A reduction of 21% on TPO antibodies is reported with the dietary intake of 0.2 mg of selenium.Increased dietary selenium reduces the effects of mercury toxicity, although it is effective only at low to modest doses of mercury. Evidence suggests that the molecular mechanisms of mercury toxicity includes the irreversible inhibition of selenoenzymes that are required to prevent and reverse oxidative damage in brain and endocrine tissues. An antioxidant, selenoneine, which is derived from selenium and has been found to be present in the blood of bluefin tuna, is the subject of scientific research regarding its possible roles in inflammatory and chronic diseases, methylmercury detoxification, and oxidative damages. It seems as though when mercury levels in a marine fish rise, so do the selenium levels. To the knowledge of researchers, there are no reports of mercury levels exceeding that of selenium levels in ocean fish. Evolution in biology
From about three billion years ago, prokaryotic selenoprotein families drive the evolution of selenocysteine, an amino acid. Selenium is incorporated into several prokaryotic selenoprotein families in bacteria, archaea, and eukaryotes as selenocysteine, where selenoprotein peroxiredoxins protect bacterial and eukaryotic cells against oxidative damage. Selenoprotein families of GSH-Px and the deiodinases of eukaryotic cells seem to have a bacterial phylogenetic origin.