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Trichloroethene-induced autoimmune response in female MRL +/+ mice.
The results suggest that TCE and its metabolite, DCAC, induce and/or accelerate autoimmune responses in female MRL +/+ mice and suggests that this metabolite may be important in the mechanisms leading to TCE-induced autoimmunity. Expand
Curcumin-glutathione interactions and the role of human glutathione S-transferase P1-1.
The presence of recombinant human glutathione S-transferase(GST)P1-1 significantly accelerated the initial rate of GSH-mediated consumption of curcumin in 10 mM potassium phosphate, pH 7.0, and 1 mM GSH and was shown to catalyze the reverse reaction leading to the formation ofCurcumin from GSH adducts of FMK and FAL. Expand
Markers of oxidative and nitrosative stress in systemic lupus erythematosus: correlation with disease activity.
The stronger response observed in serum samples from patients with higher SLEDAI scores suggests that markers of oxidative/nitrosative stress may be useful in evaluating the progression of SLE and in elucidating the mechanisms of disease pathogenesis. Expand
Interactions of glutathione S-transferase-pi with ethacrynic acid and its glutathione conjugate.
Results of these studies suggest that inhibition of GSTs by ethacrynic acid-GSH conjugate may be the main mechanism through which ethacRYnic acid reverses alkylating agent resistance. Expand
Anti-malondialdehyde antibodies in MRL+/+ mice treated with trichloroethene and dichloroacetyl chloride: possible role of lipid peroxidation in autoimmunity.
Trichloroethene (TCE) and one of its metabolites dichloroacetyl chloride (DCAC) are known to induce/accelerate autoimmune (AI) response in MRL+/+ mice as evident from anti-nuclear, anti-ssDNA,Expand
Chronic exposure to trichloroethene causes early onset of SLE-like disease in female MRL +/+ mice.
It is suggested that chronic exposure to TCE promotes inflammation in the liver, pancreas, lungs, and kidneys, which may lead to SLE-like disease in MRL +/+ mice. Expand
Metabolic basis of ethanol-induced hepatic and pancreatic injury in hepatic alcohol dehydrogenase deficient deer mice.
Although the present studies clearly indicate a metabolic basis of ethanol-induced hepatic and pancreatic injury, detailed dose- and time-dependent toxicity studies in this ADH(-) deer mouse model could reveal further a better understanding of mechanism(s) of alcohol-induced liver disease and pancreatitis-like injuries. Expand
Further investigations of mutagenic cholesterol preparations.
The previously demonstrated mutagenicity of naturally air-aged (autoxidized) USP cholesterol in test strains of Salmonella typhimurium has been confirmed, and themutagenic species from mutagenic cholesterol preparations were shown to be neutral steroids that are very much more polar than the cholesterol autoxidation products so far identified. Expand
Oxidative and nitrosative stress in trichloroethene-mediated autoimmune response.
It is suggested that TCE exposure not only leads to oxidative/nitrosative stress, but is also associated with induction/exacerbation of autoimmune response in MRL+/+ mice. Expand
Metabolic basis of ethanol-induced cytotoxicity in recombinant HepG2 cells: role of nonoxidative metabolism.
The results suggest that ADH-catalyzed oxidative metabolism of ethanol is the major mechanism of its disposition, regardless of CYP2E1 overexpression and strongly support the hypothesis that diminished hepatic ADH activity facilitates nonoxidative metabolism ofanol and the products of ethanol nonoxIDative metabolism cause apoptosis in HepG2 cells via intrinsic pathway. Expand