Heterozygous SOD1 deficiency in mice with an NZW background causes male infertility and an aberrant immune phenotype.

Heterozygous SOD1 deficiency in mice with an NZW background causes male infertility and an aberrant immune phenotype. Free Radic Res. 2019 Oct 08;:1-341 Authors: Homma T, Takeda Y, Sakahara S, Ishii N, Kobayashi S, Abe H, Asao H, Fujii J Abstract New Zealand white (NZW) mouse is a mutant strain that has a larval defect in the immune system, and an F1 hybrid between NZW and New Zealand Black mouse spontaneously develops systemic lupus erythematosus (SLE). In meantime the ablation of superoxide dismutase 1 (Sod1) causes autoimmune hemolytic anemia, a clinical condition of SLE, in mice with a C57BL/6 background. Based on our previous studies, we hypothesized that oxidative stress may trigger this aberrant autoimmunity in NZW mice without crossing with another strain. To validate this, we attempted to establish Sod1-/-/NZW mice but this attempt failed to obtain any objective mouse. The congenic Sod1+/-/NZW male mice were completely infertile because of severe oligozoospermia attributed to a defect in spermatogenesis. The levels of the SOD1 protein were about a half in the testes of the Sod1+/-/NZW mice. Sperm from the Sod1+/-/NZW mice were largely defective and showed quite low fertilizing ability in in-vitro fertilization assays. Concomitant with an increase in the oxidatively modified proteins, spermatogenic cells underwent more cell death in the testes of the Sod1+/-/NZW mice compared to those of WT/NZW mice. An examination of immunoc...
Source: Free Radical Research - Category: Research Tags: Free Radic Res Source Type: research