SOD1 and amyotrophic lateral sclerosis: In addition, these studies suggested that H2O2 formed by overexpression of humanSOD1 (hSOD1) is efficiently destroyed, whereas more of H2O2 produced by the mSOD1 escapes into the tissue where it may produce damaging HO•, thereby causing the oxidation of protein, DNA, and membrane phospholipids causing motor degeneration in ALS.