Liver detoxifying function

More recently, an indirect method of electrochemical detoxification of organisms has been put into practice. It is based on a model of the detoxifying function of the liver. A normal liver produces cytochrome P450, which assures the hydroxylation... 

Hepatic Effects. No studies were located regarding hepatic effects in humans after inhalation exposure to barium. Impaired detoxifying function of the liver was noted in one study in which rats were treated by intermediate inhalation exposure to 3.6 mg barium/m as barium carbonate dust (Tarasenko et al. 1977). No other details were reported. 

Of the twelve metabolic functions shown in table 3.1, both the biotransformation and the detoxifying function are of major relevance. Disturbance of one or several of the other metabolic fields may be hazardous and is often associated with complications - any breakdown of the detoxifying function, however, leads to cell necrosis and liver failure, and thus death. 

A.3.2 The liver is an organ with many functions and the very definition of its metabolic state can be very complicated. Some of the major functions of the liver are to produce enzymes to break down fats and proteins and the conversion of sugars into proteins and vice versa. The liver makes most amino acids and will process nitrogen waste to make urea, which is excreted in the urine. The liver detoxifies many materials that are ingested and will metabolize drugs and alcohol. It stores certain vitamins, breaks down hemoglobin (from red blood cells) and maintains the level of glucose in the blood. It also makes 80% of the cholesterol in the body. 

Certain flavonoids isolated from Helichrysum flowers (especially quercitrin, kaempferol, naringenin, and isohelichrysin) have been reported to increase bile secretion in experimental animals. Quercitrin also increased the detoxifying function of the liver and exhibited an anti-inflammatory activity. ... 

In liver disease, for example, the ability to metabolize or detoxify a specific type of drug may be impaired. If the average or normal dose of the drug is given, the liver may be unable to metabolize the drug at a normal rate Consequently, the drug may be excreted from the body at a much slower rate than normal. The primary health care provider may then decide to prescribe a lower dose and lengthen the time between doses because liver function is abnormal. 

No studies were located indicating that any populations are unusually susceptible to heptachlor or heptachlor epoxide. There is a possibility that very young children may exhibit particular susceptibility to hepatic effects because of the immaturity of the hepatic microsomal system. Heptachlor is bioactivated to produce heptachlor epoxide which is more toxic than heptachlor. Preadolescent children have a greater rate of glutathione turnover, and they are expected to be more susceptible to heptachlor epoxide-induced toxicity. Their susceptibility would probably depend upon their ability to detoxify heptachlor epoxide. Individuals who show reduced liver function for other... 

Acetyls alley lie acid was shown to prevent cirrhosis under certain experimental conditions [125]. Naproxen and indomethacin partially protected against LPS and D-galactosamine-in-duced hepatotoxicity [126] Acetylsalicylic acid and ibuprofen were also protective in endo-toxic shock [127]. Endotoxaemia is one of the complications in cirrhotic patients [128] and is probably caused by an impaired ability of the liver to take up and detoxify gut-derived LPS [116]. The presence of portosystemic shunts in cirrhotic patients may also contribute to this spill-over of LPS into the systemic circulation [129]. NSAIDs, however, are also reported to provoke deleterious effects on renal function in cirrhosis [130], and can therefore not be used in cirrhotic patients. Cell-specific delivery of NSAIDs to SECs and/or KCs may make application of these drugs in cirrhosis feasible by circumventing the renal side-effects. 

The liver is the central organ that filters, stores, and detoxifies blood and its constituents. Thus, it is highly susceptible to a host of injuries because of its portal location and physiologic function. Blood distribution gradient exists within the liver and this heterogeneity results in differential exposure of various parts of the organ to injury. Hepatocytes closest to the portal vein and hepatic artery receive oxygen- and nutrient-rich blood supply, which makes them less susceptible to injury than those distal to blood supply [2]. 

The metabolic and clinical condition of the patient also plays a role The individual with good kidney and liver function will respond quite differently to a drug than the patient who is not able to detoxify or excrete the compound. The user of laboratory data must be aware of the possible occurrence of drug-mediated enzyme induction, biological variations in the rate of clearance and storage in depot areas (B24), and the genetic factors that play a role in the toxicity of a drug (L2). 

The mammalian liver is a construction of living cells that function (unlike in other organs) in a delicate choreography that simultaneously detoxifies, metabolizes, and synthesizes proteins. The liver handles the breakdown and synthesis of carbohydrates, lipids, amino acids, proteins, nucleic acids, and coenzymes (Figure 1.8). In addition to the hepatocytes, other cells within the liver perform other vital functions. The system contributes to the disposition of particulates carried by the bloodstream and fights myriad microbiological agents responsible for a number of infectious diseases. ... 

We have not pursued mechanisms but suggest that the enhancement of carcinogenesis may be related to a role for riboflavin in the activation of enzymatic processes involved with metabolic detoxification of MBN, similar to azo reductase and its role in the detoxification of 4-dimethylaminoazobenzene (32). In this case riboflavin activates azo reductase in the liver and this, in turn, is associated with decreased carcinogenicity. Conversely, when animals are deprived of riboflavin, there is less active enzyme present to detoxify the chemical and the induction of liver cancer is enhanced. A similar process may be functioning in our MBN, riboflavin deprived model but the exact nature of the mechanism requires additional research. 

The threshold for toxic effects occurs at the point where the body s ability to detoxify a substance or repair toxic injury has been exceeded. For most organs there is a reserve capacity in such a way that the loss of some organ function does not decrease performance. For example, the development of cirrhosis in the liver may not result in a clinical effect until over 50% of the liver has been replaced by fibrous tissue. 

Intoxication bypolfaesis Substances which impair or damage the functioning of the central nervous system are inadequately detoxified by the diseased liver and/or pass the liver unaltered by way of existing collateral circulatory pathways. Differentiation should be made here between (I.) ammonia-induced neurotoxicity and (2.) synergistic neurotoxic interaction between ammonia, mercaptans, short-chain fatty acids and phenols. 

However, if paracetamol is taken in overdose, the levels of quinoneimine exceed the ability of glutathione to convert it back to paracetamol and toxicity to the liver results. In some cases, if treatment is not initiated in time, severe toxicity results, leading to death by acute liver failure. Treatment of paracetamol overdose is by administration of N-acetylcysteine (Figure 5.8). This compound (the acetyl derivative of the essential amino acid cysteine) functions as an alternative source of thiol (—SH) groups, which act in a similar manner to glutathione to detoxify the quinoneimine. 

A primary function of the liver and kidneys is to detoxify and clear poisonous substances from the body. For these reasons, they are often the first to be affected by the use of toxic herbs. A number of reviews address the global... 

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