Fatty change

Hepatic Effects. Liver lesions have been reported in humans acutely intoxicated by methyl parathion formulation (Wolfatox) (Fazekas 1971 Fazekas and Rengei 1964). These studies are discussed in detail in Section 3.2.2.1. Liver lesions were hepatocellular swelling, degeneration, and fatty change. 

M (increased incidences of clear cell foci, fatty change, and ceroid pigmentation)... 

Rat Sprague- Dawley 10 wk ad lib (F) Hepatic 500 M (mild fatty change, increased gamma glutamyl-transpeptidase + foci) DeAngelo et al. 1986 X m T T m 3 to... 

An MRL of 0.4 mg/kg/day has been derived for intermediate-duration oral exposure to di-/ -octylphthalate. This MRL is based on a NOAEL of 40.8 mg/kg/day for liver effects that were observed in rats fed di-w-octylphthalate in the diet at a dose of 350.1 mg/kg/day (males) or 402.9 mg/kg/day (females) (Poon et al. 1995). These hepatic effects consisted of a statistically significant (p<0.05) increase in hepatic ethoxyresorufin-0-deethylase activity and histological changes in hepatic architecture, including accentuation of zonation and perivenous cytoplasmic vacuolation. Thyroid toxicity (decreased colloid density and reduced follicle size) was also noted at this concentration. The NOAEL was divided by an uncertainty factor of 100 (10 for extrapolation from animals to humans and 10 for human variability). Support for the use of hepatic toxicity as the basis of the intermediate MRL is provided by other studies that show necrosis and other fatty changes after acute- and intermediate-duration exposure of rats (DeAngelo et al. 1986 Lake et al. 1984, 1986 ... 

Other additional studies or pertinent information which lend support to this MRL The choice of liver toxicity as the basis of the MRL is supported by necrosis and mild hepatic fatty changes seen in other acute- and intermediate-duration studies in rats (DeAngelo et al. 1986 Lake et al. 1984, 1986 Mann et al. 1985). 

Hepatic 26 (fatty changes, centrolobular degeneration and necrosis)... 

Acute toxic hepatic effects of 1,2-dibromoethane consisting of hepatocellular cloudy swelling, centrilobular fatty change, and patchy necrosis were reported in animals after a single inhalation exposure (Rowe et al. 1952). Repeated inhalation exposures of rats and rabbits to 100 ppm... 

Rats in a subchronic inhalation study exposed to 50 ppm 1,2-dibromoethane had intercurrent infectious disease that severely complicated experimental results (see the discussion in this section on Respiratory Effects). No liver lesions were reported in surviving rats (Rowe et al. 1952). Guinea pigs exposed to 50 ppm 1,2-dibromoethane did not develop respiratory disease. Their liver lesions consisted of minimal centrilobular hepatocellular fatty change (Rowe et al. 1952). Liver lesions were not induced in F344 rats or B6C3i mice following subchronic exposure to any concentrations of... 

Dibromoethane is considered to be a weak hepatotoxin in animals. Hepatocellular fatty change (degeneration) is one of the common lesions in experimental animals associated with acute oral exposure to 1,2-dibromoethane (Botti et al. 1986). When administered to rats by gavage at a dosage of 110 mg/kg/day, this lesion is corroborated by an increase in liver triglyceride levels that begins within 8 hours of treatment (Nachtomi and Alumot 1972). 

Using light microscopy, Broda et al. (1976) did not observe hepatocellular fatty change in livers of rats exposed by gavage to 110 mg/kg 1,2-dibromoethane in olive oil. Rats developed centrilobular dilatation within 8 hours after exposure, hepatocellular degeneration within 17 hours after exposure, and frank centrilobular necrosis 22 hours after 1,2-dibromoethane exposure. 

Little information exists about the mechanism of action of the azaspiracids. The chronic effects observed in mice after oral administration of azaspiracid included interstitial pneumonia, shortened villi in the stomach and small intestine, fatty changes in the liver, and necrosis of lymphocytes in the thymus and spleen (Ito et al., 2002). 

Mouse once Hepatic 35 (midzonal fatty changes) 350 (centrilobular necrosis) Jones et al. 1958... 

Mouse 90 d Hepatic 60 (fatty changes) 270 (cirrhosis) Bulletal. 1986... 

F (increased plasma GPT levels fatty changes in liver in 1/6)... 

Exposure of rats 7 hours/day, 5 days/week for 6 months at 0.1 ppm caused no effects. Exposure at higher but unstated levels caused poor growth and fatty changes in the liver. In the eyes of rabbits the material caused severe irritation and irreversible corneal damage. The vapor is a lacrimator. On the skin of rabbits it caused slight irritation. 

The LCso for a 7-hour exposure of mice was 18,354ppm. Exposure 7 hours/day to 11,300 ppm for 1 week caused mild eye and nose irritation, incoordination, and light narcosis after 4 hours the exposure was fatal to 6 of 50 mice. Animals exposed to toxic concentrations often developed marked fatty changes in the liver, kidney, and heart and inflammatory changes in the lungs. Rats were unaffected by eight 6-hour exposures to 4000 ppm. ... 

In a carcinogenicity study, Swiss mice were exposed to 10 or 2 5 ppm 4 hours/day, 5 days/ week for 52 weeks. After 98 weeks, 2 5 ppm had caused kidney adenocarcinomas in 24 of 150 males and 1 of 150 females whereas none were seen in the control group. Rats exposed to 75 ppm 6 hours/day, 5/days week for 18 months and then held until 24 months showed a reversible hepatocellular fatty change but no increase in tumor incidence that could be attributed to VDC exposure. Several other studies in other strains of mice, rats, and hamsters did not produce carcinogenic effects. ... 

Valdivia E, Sonnad J. 1966. Fatty change of the granular preumocyte in carbon tetrachloride intoxication. Arch Pathol 81 514-519. 

For alcoholic hepatitis is no specific treatment beyond alcohol withdrawal. Corticosteroids have no value. Fatty change in the liver is common, but should not be confused with fatty change associated with non-alcoholic disease, notably diabetes melli-tus. 

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