Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing a familial amyotrophic lateral sclerosis mutant SOD1
Store in a cool, dry place for optimal efficacy
In comparison, the ORO-positive lesions in the aortas of mice treated with Mn/TI@mHSA, P-Mn@mHSA, or P-Mn/TI@mHSA-N were notably diminished
Because human studies are limited, doctors do not yet have clear data on the peptide's long-term effects, optimal dosing, potential drug interactions, or safety across different patient populations
It is known that free radicals are responsible for diseases such as atherosclerosis, diabetes, epilepsy, inflammatory diseases and cancer