Key result
Heterozygous MnSOD knockout mice show similar survival in 100% oxygen versus normal littermates.
Why the study?
Heterozygous MnSOD gene-knockout mice are phenotypically normal in room air, but their susceptibility to 100% oxygen toxicity was unclear.
Does heterozygous MnSOD gene knockout increase susceptibility to 100% oxygen toxicity in mice?
Comparison
Sod2(+/-) mice vs Sod2(+/+) littermates exposed to 100% O2
Design
Preclinical experimental study
Follow-up
Mean survival time until death (~101-103 hours)
Authors
Loading...
50% MnSOD activity suffices for normal hyperoxia resistance in mice; leaves open complete knockout effects and human translation.
Does heterozygous MnSOD gene knockout increase susceptibility to 100% oxygen toxicity in mice?
Absolute Event Rate: 101.4% vs 103.2%
p-value: p=> 0.60
In mice, 50% of normal MnSOD activity appears sufficient to maintain normal resistance to 100% oxygen toxicity and prevent myocardial ultrastructural abnormalities.
Tsan et al. (1998) studied Oxygen toxicity (n=40). Heterozygous MnSOD gene-knockout (Sod2+/-) vs. Normal Sod2(+/+) littermates was evaluated on Survival in 100% O2 (hours) (p=> 0.60). Heterozygous MnSOD gene-knockout mice (Sod2+/-) had similar survival in 100% oxygen compared to normal littermates (101.4 vs 103.2 hours; P>0.60).
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: