Fatty degeneration of the liver

Intermediate-duration inhalation studies were all single concentration studies at concentrations that resulted in serious effects (26-52 ppm) (Deichmann et al. 1944), or no effects (5 ppm) (Sandage 1961). Therefore, an intermediate-duration inhalation MRL was not derived for phenol. The serious effects noted included pneumonia, necrosis of the myocardium, fatty degeneration of the liver, glomerular degeneration, and hindlimb paralysis (Deichmann et al. 1944). Additional inhalation studies that... 

Livers from toxin-injected mice showed severe congestion whether or not the mice survived the initial critical 2-hour post injection period. Occasionally, a mouse injected with a nominally lethal dose of toxin-LR survived the critical two hours but remained listless until it died several hours or several days later. The reasons for the delayed death are unknown. Such mice developed focal fatty degeneration of the liver and active regeneration of liver cells. 

After a single exposure of rabbits to 17 ppm for 6 hours, the sensory trigeminal nucleus was severely affected. Other effects included tubular and focal necrosis in the collecting tubules of the kidney and fatty degeneration of the liver. ... 

The oral LDso in rats has ranged from 0.71 ml/kg to 2.83 g/kg. The effects of intraperi-toneal administration to rats of doses of 100 or 500 mg/kg were assessed at 4 and 24 hours after dosing.In the liver and kidneys, there was qrtoplasmic vacuolization. The high doses caused renal tubular degeneration. In rats fed 0.17g/% for 90 days, effects included cloudy swelling and degeneration of kidney tubules and fatty degeneration of the liver. ... 

The former use of ethyl bromide as a human anesthetic (at concentrations approaching 100,000 ppm) produced respiratory irritation and caused some fatalities, either immediately, due to respiratory or cardiac arrest, or delayed, due to effects on the liver, kidneys, or heart. At autopsy, findings were pulmonary edema and marked fatty degeneration of the liver, kidneys, and heart. Relatively little experience with this substance in industry has been reported, but exposure of volunteers to 6500 ppm for 5 minutes produced vertigo, slight headache, and mild eye irritation. ... 

Hydrazine is absorbed through the skin. In one case attributed to hydrazine hydrate exposure, systemic effects included weakness, vomiting, excited behavior, and tremors the chief histologic findings were severe tracheitis and bronchitis, fatty degeneration of the liver, and nephritis. ... 

Rats that received a single lethal dose of NDPA showed centrilobular necrosis and fatty degeneration of the liver. Specific doses that caused this effect were not listed, but the oral LD50 was determined to be 480 mg/kg. 

Limited information is available on the effects of chronic propene exposure. In mice, chronic exposure to minimal narcotic concentrations caused moderate to very slight fatty degeneration of the liver. 

Hepatoxicity, fatty degeneration of the liver, and pancreatitis occur rarely. 

In other studies of cats, inhalation or cutaneous treatment with NG resulted in rapid formation of methemoglobin and of Heinz bodies on red blood cells. With rather low level daily subcutaneous injections (O.lmg/kg) for 40 days, one particular cat suffered anemia and fatty degeneration of the liver, followed by death yet 50 daily doses of 7.5 or 15mg/kg was survived by the majority of a group of cats. Air saturated with NG (0,6ppm) produced only anemia and moderate leukocytosis in 68 days inhalation for 156 days produced tolerance in cats... 

On the other hand, obesity in fish, especially fatty degeneration of the liver, is a sign of disturbed metabolism (Faktorovich, 1967 Sidorov, 1983). 

Stroganov (1979) and Sidorov (1983) shed new light on viral and parasitic diseases in fish. In particular, it was found that many pathological infections affected the lipid metabolism. In some cases they led to a sharp fall in the reserve lipid content, and in others to excessively high values - the so-called fatty degeneration of the liver. The proportions and quantities of structural lipids are inevitably changed in one or another direction as soon as any pathology appears. 

The accidental application of a 25% solution of chlordane (technical grade) to a human caused symptoms within 40 minutes and death before medical attention was obtained. Two patients died after the ingestion of low oral doses of chlordane. Both showed severe fatty degeneration of the liver (ref. 99. P> 550). 

The symptoms of acute and chronic poisoning by arsenic have been described by Rentoul and Smith [10], Davidson and Henry [11] and Fowler [12]. Acute symptoms include gastrointestinal damage, convulsions and haemorrhage at autopsy, fatty degeneration of the liver and kidneys is frequently noted. Acute inhalation of arsine is followed by extensive haemolysis, haemoglobinuria and death from renal failure. 

Fig. 8.4 Segmental fatty degeneration of the liver (2 = 37.3 HU) following application of CM compared with liver parenchyma of normal density (1 = 68.5 HU), and the spleen (3)...

Lipid peroxidation Free radicals induce peroxidation of the unsaturated fatty acids of the ER. As a result, there is fatty degeneration of the liver, whereby the mitochondria and biomembranes are damaged (possibly leading even to cell death). 

Inhibition of p-oxidation The enhanced formation of mitochondrial oxygen radicals in the presence of fatty degeneration of the liver causes lipid peroxidation, which can lead to steato-hepatitis and fibrosis or cirrhosis. 

Inhibition of protein synthesis Some substances can inhibit RNA polymerase II and in (s. fig. 3.5). This in turn impairs the synthesis of enzymes, structural proteins and apolipoproteins. The result is fatty degeneration of the liver and cell necrosis. 

Histologically, non-alcoholic steatohepatitis shows moderate to high-grade, mainly macrovesicular fatty degeneration of the liver cells with inflammatory infiltrates and formation of fibrosis. Cirrhosis frequently develops. Despite the morphological similarity to alcohol-induced fatty liver hepatitis, there is no (noteworthy) alcohol consumption involved in NASH. Viral or autoimmune hepatitis are not detectable either. There are no or only moderate subjective complaints. The transaminases are normal or slightly increased. NASH is mostly associated with obesity and/or type II diabetes, thus NASH is regarded as the hepatic manifestation of a metabolic syndrome. 

Ethyl bromide causes irritation and has a tendency to cause fatty degeneration of the liver, renal tissue, and the heart. 

Rabbits exposed for 8 months to vanadium pentoxide dusts showed some fatty degeneration of the liver (Sjoeberg 1950). However, liver function was not tested, and the author stated, without explanation, that the liver changes were of no special significance. 

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