dimethyl sulfoxide/necrosis

Extravasation of Adriamycin during i.v. infusion can cause serious local complications. We have used a rat skin model to study the protection afforded by dimethyl sulfoxide and alpha-tocopherol (vitamin E) against Adriamycin-induced skin necrosis. Topical daily application of 1 ml dimethyl sulfoxide

Dimethyl sulfoxide (DMSO) is evident to induce apoptosis in certain tumor cells in vitro. However, its apoptotic mechanism remains unexplored in in vivo tumors. This article describes that DMSO, being non-toxic to the normal lymphocytes, up regulated TNFα and p53, declined Bcl-2/Bax ratio, activated

D-Galactosamine (D-Galn: 300 mg/kg) was intraperitoneally administered to rats. After 6 h the activity of plasma GOT and GPT was significantly higher than that of the control group and plasma GOT and GPT activities increased thereafter. These results indicated that the necrotic process was initiated

OBJECTIVE Without proper medication for the treatment of diabetic retinopathy, retinal cells become malnourished and degenerate, which results in damage to vision cells and can lead to blindness. Flavonoids such as biochanin A (BCA) can directly target various facets of angiogenesis. We assessed the

Previous studies performed in our laboratory indicated that non-toxic concentrations of peroxynitrite nevertheless commit U937 cells to a rapid necrosis that is however prevented by a survival signaling driven by cytosolic phospholipase A(2)-released arachidonic acid. Toxicity was mediated by

After a 30 minute period of superior mesenteric artery occlusion in adult rats, there was a significant decrease in peritoneal inflammatory reaction, ileus, peritoneal adhesion formation, and histologically proved bowel wall necrosis in animals given intravenous dimethyl sulfoxide at the end of the

The possible effect of dimethyl sulfoxide upon the development of lesions in the gray matter after experimental spinal cord trauma has been investigated with the use of cytochrome oxidase assay and quantitative histologic measurement of total liquefaction necrosis. Observations were made in 17

Granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), gamma-interferon (gamma-IFN), or tumor necrosis factor-alpha (TNF-alpha) triggered the rapid, stable phosphorylation of a 75-Kd protein (p75) when incubated with permeabilized HL60 human myeloid

Exposure to a nontoxic dose of bacterial endotoxin (lipopolysaccharide [LPS]) potentiates the hepatotoxicity of aflatoxin B(1) (AFB(1)). Because some of the pathophysiologic effects associated with LPS are mediated through tumor necrosis factor alpha (TNF-alpha), this study was conducted to explore

The prevention and treatment of vesicant extravasation presents unique nursing challenges. In two case studies, the authors describe the clinical response of patients to dimethyl sulfoxide after multivesicant extravasation. The patients studied did not experience deep tissue necrosis or resultant

Experimental lens-induced uveitis was produced in Lewis rats by sensitization with bovine lens protein prior to disruption of the lens capsule. Treatment of these animals by intraperitoneal injection of dimethyl sulfoxide resulted in reduction in retinal vasculitis, hemorrhage and necrosis.

Experiments with two models of intestinal ischemia were performed in order to examine the protective effect of dimethyl sulfoxide (DMSO). Segmental ischemia of the small intestine for 150 minutes caused necrosis of the affected bowel in 90% of the animals. Intravenous administration of DMSO or

There is ample evidence of the involvement of free radicals in mediating skin flap necrosis. Dimethyl sulfoxide (DMSO) is a well-tolerated, safe drug that is a powerful scavenger of the hydroxyl free radical. The current study investigated the effect of DMSO on the survival of 9 x 4 cm skin flaps

BACKGROUND Accidental extravasation of doxorubicin leads to skin necrosis and significant morbidity. Based on our previous work in the rat, we hypothesized that the free radical scavengers dimethyl sulfoxide (DMSO) and vitamin C prevent doxorubicin-induced skin ulcers in white swine. METHODS Fifteen

Dimethyl sulfoxide (DMSO) is a widely used prototypical chemical inducer of cell differentiation. In the present study, the effects of DMSO on susceptibility of human myeloid leukemia U937 cells towards ligation of distinct death receptors (DRs) were investigated. DMSO sensitized cells towards