Intraperitoneal ascorbic acid

In a study with experimental animals (62), both ascorbic acid (2.5 mM/kg dose) and zinc as zinc sulfate (1.4 mM/kg dose) increased ethanol clearance from the blood of intoxicated, 250-g rats when sterile solutions of the respective compounds were injected intraperitoneally. The effects appeared to be independent, because neither additive nor synergistic effects on clearance were noted when the two agents were injected simultaneously. 

Enhanced excretion of vanadium was achieved with chelation therapy provided by deferoxamine mesylate (DFOA) (Gomez et al. 1988). Humans or animals with vanadium poisoning have not been helped by the chelating agent dimercaprol (BAL), which is often effective in lessening the toxicity of other metals (Lusky et al. 1949). Intraperitoneal injections of ascorbic acid and of ethylene diamine tetraacetate (EDTA) reduced vanadium-induced morbidity in mice and rats (Jones and Basinger 1983 Mitchell and Floyd 1954). 

Ascorbic acid and sodium ascorbate have been reported to prevent toxicity of morphine in mice (Dunlap and Leslie 1985). Sodium ascorbate (1 g/kg) injected intraperitoneally 10 minutes before morphine (500 mg/kg) protected the animals against mortality due to respiratory depression. These investigators postulated that ascorbate antagonized the toxicity of morphine by selectively affecting the neuronal activity. 

In contrast to ascorbic acid and a-tocopherol amidothionophosphates did not have any prooxidative effects as measured by oxygen consumption from buffer solutions containing the drug and cupric sulphate as a source of redox-active metal ions (Ti-ROSH et al. 1996). Amidothionophosphates reduced significantly and in a dose-dependent manner the oxygen burst in human neutrophils as measured by luminol-dependent luminescence, and they also markedly depressed the killing of human fibroblasts by mixtures of glucose oxidase and streptolysin S. The toxicity of these molecules was tested by intraperitoneal injection of doses up to 1000 mg/kg to white Sabra mice. No mortality was observed 30 d after administration of up to 500 mg/kg. 

The intraperitoneal injection of massive doses of uric acid has been reported to produce a transitory hyperglycemia when this compound was administered to GSH-depleted rabbits (32). The diet fed was low in cysteine and methionine but it was supplemented with 0.1 % ascorbic acid. When the fall in blood GSH level was prevented by methionine supplementation of the diet, uric-acid injection failed to induce diabetes (32). 

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