Abstract

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.

Highlights

  • Type I diabetes, often called juvenile diabetes, results from the loss of active insulin-producing pancreatic-beta cells which causes an insulin deficit

  • It is clear that previous approaches of controlling blood sugar levels or insulin levels has not been very effective, since the diabetic disease process continues

  • This is because the basis of the disease process, oxidative/nitrosative stress, has never been addressed

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Summary

Introduction

Type I diabetes, often called juvenile diabetes, results from the loss of active insulin-producing pancreatic-beta cells which causes an insulin deficit. Excessive glucose in the blood and the loss of insulin produces vascular damage via glycosylation and activation of oxidative and nitrosative stress linked to all of the symptoms associated with diabetes, including peripheral and autonomic neuropathy, nephropathy, and retinopathy. Chemical attack that produces nitric oxide and superoxide that may form peroxynitrite could be involved from recent experiments done by a variety of investigators [2,3,4,5] This same aforementioned chemical scenario is very likely to be the destructive chemistry seen in genetic and virally induced type I diabetes

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