methyl ethyl ketone/necrosis

The plastic hardener methyl ethyl ketone peroxide is unstable peroxide that releases free oxygen radicals. Ingestion of this compound induces widespread liver necrosis, severe metabolic acidosis, corrosive esophagitis and gastritis, that is often fatal. A 49-year-old man unintentionally ingested

Fatal massive peripheral zonal hepatic necrosis developed in a 47-year-old man who accidentally ingested a solution of methyl ethyl ketone peroxide (MEKP) in dimethyl phthalate. Such solutions contain about 10% active oxygen. The clinical course was characterized by temporary cardiac arrest,

OBJECTIVE To investigate the pathological changes of major organs in rats that have inhaled methyl ethyl ketone peroxide (MEKP) aerosol and to provide clues to the oxidative damage mechanism of MEKP. METHODS A total of 100 Sprague-Dawley rats (male-to-female ratio = 1:1) were randomly and equally

OBJECTIVE To investigate the effects of an acute exposure to 200 ppm methyl ethyl ketone on the nasal mucosa of healthy volunteers. METHODS Nineteen healthy non-smoking men were exposed to 200 ppm methyl ethyl ketone and to a sham exposure in an exposure chamber, using a cross-over design.

Methyl ethyl ketone peroxide (MEKP) is a free radical-generating compound used as a fiberglass resin hardener. A 41-year-old Haitian man developed severe metabolic acidosis, hemolysis, esophageal and gastric necrosis, and perforation of the stomach after drinking an undetermined amount of MEKP in a

Methyl ethyl ketone peroxide (MEKP) is an unstable organic peroxide used in the manufacture of acrylic resins, as a hardening agent for fiberglass-reinforced plastics, and as a curing agent for unsaturated polyester resins. It is commercially available as a 40% to 60% solution in dimethyl phthalate

The plastic hardener methyl ethyl ketone peroxide (MEKP) is an unstable peroxide that releases free oxygen radicals. Ingestion of this compound induces widespread liver necrosis that is often fatal, extensive ulceration with subsequent scarring, and stenosis of the proximal digestive tract in

The aim of this research was to improve our understanding of human toxicity due to exposure to DMF, MEK, or TOL individually as compared to exposure to DMF-MEK or DMF-TOL mixtures, by comparing EC50 values as well as the morphological changes in HepG2 cells treated with these substances. We found

To evaluate the oncogenic potential of methylethylketoxime (MEKO), CD-1 mice (50/sex/group) and F-344 rats (50/sex/group) were coexposed 6 h/day, 5 days/wk for 18 mo (mice) or 26 mo (rats) via whole-body inhalation exposures to target vapor concentrations of 0, 15, 75, and 375 ppm (actual