Can diabetes I and early blindness be prevented using a tylenol combination which inhibits oxidative and nitrosative stress?

Since oxidative/nitrosative stress cause diabetes, can we prevent this chemistry generating the disease? Streptozotocin causes diabetes by entering the pancreatic beta cell generating excessive nitric oxide which reacts with oxygen creating a toxin possibly peroxynitrite, dinitrogen trioxide, dinitrogen tetraoxide and so forth. The toxic compounds damage the DNA causing beta cell death. This prevents insulin synthesis, storage and release. By using antioxidant substances that destroy the nitric-oxide-based toxins (e.g., carboxy-PTIO (oxidizes nitric oxide), polyphenolic-quercetin and monophenolic acetaminophen (Tylenol)) which are oxidation and nitration targets can the diabetes I causing toxins in animals be destroyed? Will this tri-drug combination completely prevent the deleterious effects of diabetes namely poor blood glucose control and blindness from cataracts for the entire length of the experiment (one year). These disease reversal experiments were accomplished in rats where the streptozotocin-diabetic effects were completely thwarted. In vitro experiments were accomplished to provide the scientific basis for the experimental results in animals.

Oxidative/nitrosative stresses trigger type I diabetes: preventable in streptozotocin rats and detectable in human disease.

Recently we demonstrated that streptozotocin (STZ) diabetes (type I) in rats is preventable using a simultaneous equimolar injection of carboxy-PTIO (c-PTIO). Both changes in blood sugar and cataracts are prevented. This apparently occurs because the nitric oxide (NO) (from STZ) generated in the beta cells is oxidized to nitrite by c-PTIO preventing diabetes. STZ generates NO producing a NO-based toxin. The toxin damages DNA by nicking and activates poly-ADP-ribose causing necrosis and triggering inflammation. Is there evidence that O/N stress occurs in early human type I diabetes? We studied 40 children with or without early type I diabetes and observed that urate is decreased 25% in all these diabetic children each over the age of 3 years. Urate is a major portion of blood-antioxidant load. Surely this decrease in urate indicates ongoing O/N stress. Does O/N stress initiate disease? STZ studies in rats indicates that this is correct.