Liver tissue damage

Another common liver disease, alcoholic liver damage produced by moderate to heavy alcoholic intake, is also reflected by an elevation of the serum GOT and GPT activities. The serim glutamyl transferase activity is reported to be a sensitive index of alcoholic intake and can serve to monitor persons on alcoholic withdrawal programs (60). The LD-5 isoenzyme arises mainly from liver tissue, but has a short half-life (61), which is about 1/5 and 1/2 of the half life of the transaminases, GPT and GOT respectively. Some authors consider that a normal LD-5 isoenzyme activity in a jaundiced patient is sufficient evidence to exclude primary liver disease and that obstruction is probably responsible for the jaundice (62). In hemolytic jaundice the LDH-1 and 2 isoenzymes are elevated. 

Selden, C., Seymour, C.A. and Peters, T.J. (1980). Activities of some free radical scavenging enzymes and glutathione concentrations in human and rat liver and their relationship to the pathogenesis of tissue damage in iron overload. Clin. Sci. 58, 211-219. 

Liver Fever, lethargy, change in color or quantity of bile in patients w/ biliary T-tube, graft tenderness and swelling, back pain, anorexia, ileus, tachycardia, jaundice, ascites, encephalopathy Abnormal LFTs, increased bilirubin, alkaline phosphatase, transaminases, biopsy positive for mononuclear cell infiltrate with evidence of tissue damage... 

Monomethylhydrazine-induced mutagenesis was not observed in Ames Salmonella/ microsome with activation (Matheson et al. 1978). In vivo tests in mice (dominant lethal, revertants in host-mediated assay), and dogs (micronuclei) were negative (reviewed in Trochimowicz 1994). However, in vitro chromosomal damage in human and rat tissue has been demonstrated, although in vivo liver DNA damage (as determined by DNA alkaline elution) was equivocal (reviewed in Trochimowicz 1994). 

Arsenic vesicants produce immediate pain. Tissue damage occurs within minutes of exposure but clinical effects may not appear for up to 24 hours. Some agents are rapidly absorbed through the skin. Extensive skin contamination may cause systemic damage to the liver, kidneys, nervous system, red blood cells, and the brain. 

SOD isolated from bovine liver or erythrocytes has been used medically as an anti-inflammatory agent. Human SOD has also been expressed in several recombinant systems, and is currently being evaluated to assess its ability to prevent tissue damage induced by exposure to excessively oxygen-rich blood. 

Adults require 1-2 mg of copper per day, and eliminate excess copper in bile and feces. Most plasma copper is present in ceruloplasmin. In Wilson s disease, the diminished availability of ceruloplasmin interferes with the function of enzymes that rely on ceruloplasmin as a copper donor (e.g. cytochrome oxidase, tyrosinase and superoxide dismutase). In addition, loss of copper-binding capacity in the serum leads to copper deposition in liver, brain and other organs, resulting in tissue damage. The mechanisms of toxicity are not fully understood, but may involve the formation of hydroxyl radicals via the Fenton reaction, which, in turn initiates a cascade of cellular cytotoxic events, including mitochondrial dysfunction, lipid peroxidation, disruption of calcium ion homeostasis, and cell death. 

Some deaths. Yellow discoloration of sclera of eye passing of red-colored urine. Copper concentrations, in mg/kg DW, from sheep fed nonheliotrope diets were 1394 in liver (824 in controls) and 132 in kidney (20 in controls). Sheep on heliotrope diet had 2783 mg/kg DW in liver and 321 mg Cu/kg DW in kidney Severe morphological changes in liver, kidney, and brain tissue damage continued after cessation of copper and was sufficiently severe to lead to repeated hemolytic crises. Maximum copper concentrations at day 83 were 3289 mg/kg DW in liver (138 in controls), and 683 in kidney (15 in controls)... 

Figure 18.5 A summary of the biochemical, physiological and immunological changes brought about by cytokines in response to trauma. Cytokines can be produced in trauma from macrophages, lymphocytes, endothelial cells in the tissue that is damaged, and also by Kupffer cells if the liver is damaged. IL-1, IL-6 - interleukins 1 and 6 TNF - tumour necrosis factor, IFN - interferon.

Most cases of intoxication from industrial exposure have been mild, with rapid onset of eye irritation, headache, sneezing, and nausea weakness, light-headedness, and vomiting may also occur. Acute exposure to high concentrations may produce profound weakness, asphyxia, and death. Acrylonitrile is metabolized to cyanide by hepatic microsomal reactions. Deaths from acute poisoning result from inhibition of mitochondrial cytochrome oxidase activity by metabolically liberated cyanide. Inhalation of more moderate concentrations for a longer period of time leads to damage to the liver tissues in addition to central nervous system (CNS) effects. ... 

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