Liver damage increase

CHRONIC HEALTH RISKS possible liver damage increased risk of lung damage and chronic respiratory disease may have anticoagulant effect on the blood. 

Biochemical evidence of liver damage (increased blood glutamic oxaloacetic transaminase [GOT], glutamic pyruvic transaminase [GRT], glutamate dehydrogenase [GDH], bile acids, and cholesterol), as well as hepatocellular enlargement and vacuolation, were observed in rats exposed to 154 mg... 

TCDD is the most potent inducer of chloracne. This has been well known since the accident in Seveso, Italy, in 1976 in which large amounts of TCDD were distributed in the environment subsequent to an explosion in a factory that produced a chlorophenoxy herbicide, 2,4,5-T. TCDD is an impurity produced during the production of 2,4,5-T. The most common long-term effect of TCDD exposure was chloracne. Exposed individuals also suffered increased excretion of porphyrins, hyper-pigmentation, central nervous system effects, and liver damage and increased risk of cancer was a long-term consequence of the exposure. In addition to TCDD, polychlorinated biphenyls (PCBs), polychlorinated dibenzofurans, and polychloronaphthalens cause chloracne as well as other effects typical of TCDD. 7i... 

Hypouricemia and increased excretion of hypoxanthine and xanthine are associated with xanthine oxidase deficiency due to a genetic defect or to severe liver damage. Patients with a severe enzyme deficiency may exhibit xanthinuria and xanthine lithiasis. 

In humans, mild jaundice lasting several days to 4 weeks has been observed after acute occupational exposure to acrylonitrile vapors at high concentrations (Wilson 1944) however, the concentrations of acrylonitrile to which workers were exposed were not reported. The effects were fully reversible. In factory workers exposed to acrylonitrile for 10 years or more, Sakurai et al. (1978) reported an increase in palpable livers of workers. However, the authors considered these results to be inconclusive because the increase was not statistically significant and subjective judgments were involved. Also, blood chemistry evaluations did not indicate liver damage. 

Overproduction of free radicals by erythrocytes and leukocytes and iron overload result in a sharp increase in free radical damage in T1 patients. Thus, Livrea et al. [385] found a twofold increase in the levels of conjugated dienes, MDA, and protein carbonyls with respect to control in serum from 42 (3-thalassemic patients. Simultaneously, there was a decrease in the content of antioxidant vitamins C (44%) and E (42%). It was suggested that the iron-induced liver damage in thalassemia may play a major role in the depletion of antioxidant vitamins. Plasma thiobarbituric acid-reactive substances (TBARS) and conjugated dienes were elevated in (3-thalassemic children compared to controls together with compensatory increase in SOD activity [386]. The development of lipid peroxidation in thalassemic erythrocytes probably depends on a decrease in reduced glutathione level and decreased catalase activity [387]. 

Increased blood pressure No deaths Kidney damage Stomach and liver damage Liver and kidney damage Increased mortality... 

Increased mortality and growth retardation in 4-5 months at 35-mg/kg diet growth normal in other groups some liver damage in 25- and 35-mg/kg groups (WHO 1984)... 

Increased respiration rate in 4 days, growth reduction and liver damage in 9 days, abnormal oocyte development and reduced spermatogonia production in 18-20 days 2... 

Acetaminophen is usually well tolerated, but potentially fatal hepatotoxicity with overdose is well documented. It should be used with caution in patients with liver disease and those who chronically abuse alcohol. Chronic alcohol users (three or more drinks daily) should be warned about an increased risk of liver damage or GI bleeding with acetaminophen. Other individuals do not appear to be at increased risk for GI bleeding. Renal toxicity occurs less frequently than with NSAIDs. 

Progressive liver damage (shock liver) manifests as elevated serum hepatic transaminases and unconjugated bilirubin. Impaired synthesis of clotting factors may increase prothrombin time (PT), international normalized ratio, and activated partial thromboplastin time (aPTT). 

The liver is sensitive to hexachloroethane following both acute and longer term exposure scenarios. Evidence of effects on the liver include increased weight and centrilobular necrosis in rats and rabbits and increased serum levels of liver enzymes in sheep. There can also be fatty degeneration of the tissues and hemorrhage when damage is severe. 

Additionally, chronic drug use has been linked to neuropsychological problems that in turn make it harder to stop the cycle of abuse. Psychoactive drugs by definition affect the brain, and long-term or acute exposure to psychoactive substances can be toxic. Furthermore, we know that drug abuse can increase the risks of stroke, brain injury related to accidents, malnutrition, or liver damage, all of which can adversely affect brain function as well. 

Increase usually due to skeletal muscle, cardiac muscle, and liver damage. Not very specific unless isozymes are evaluated. 

Cytotoxicity. The liver is the primary target organ for a variety of drugs and chemicals (Hasemen et ah, 1984 Farland et ah, 1985). The prevalence of drug-and chemical-induced liver injury is of concern because some xenobiotics can produce liver damage at dose levels that are magnitudes below that which causes cell death (Plaa, 1976). Environmental and commercial chemicals can increase this effect by as much as 100-fold (Plaa and Hewitt, 1982 Plaa, 1976). Studies of early cell injury caused by exposure to a toxicant can be undertaken easily in monolayer cultures of hepatocytes, whereas early cell injury is very difficult to assess in vivo. 

The jaundice could be due to liver damage. Hepatocytes contain AST, ALT and LD red cells also contain AST and LD but do not contain significant amounts of ALT. These data suggest increased red cell destruction rather than liver cell damage and the patient was diagnosed with haemolytic anaemia. 

Oral exposure of mice to heptachlor for 92 days (10 mg/kg/day) or 180 days (5.7 mg/kg/day) increased SGPT and decreased phospholipids and total serum cholesterol (Izushi and Ogata 1990). Triglyceride content was increased at 92 days only. Evidence of liver damage was seen as a significant increase in SGPT. An increase in the liver-to-body-weight ratio was also observed. 

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