Zoning in the Liver

Metabolic zoning has proven to be a crucial concept for researchers studying hepatic metabolism over the course of time, and under different metabolic states. Metabolic zoning involves the sharing of biochemical tasks by different regions within one organ. This form of comparlmentation has been documented for gly- 

To review the curious behavior of the liver, and its handling of glucose when the liver synthesizes glycogen, it does So from gluconeogenic precursors. But when the liver oxidizes glucose, it tends to do so only to the point of pyruvate. 

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Hepatic necrosis can be classified by the zone of the liver tissue affected. Xenobiotics, such as acetaminophen or chloroform, that undergo bioactivation to toxic intermediates cause necrosis of the cells surrounding the central veins (centrilobular) because the components of the cytochrome P450 system are found in those cells in abundance. At higher doses or in the presence of agents that increase the synthesis of cytochrome P450 (inducers), the area of necrosis may incorporate the... 

Chronic idiopathic jaundice, which is characterized by heavy black pigmentation of the parenchymal cells in the centrilobular zones of the liver, differs from other forms of familial jaundice so far described in that conjugated bilirubin as well as unconjugated bilirubin is present in the plasma and bilirubinuria occurs. The type of conjugated pigment in the plasma has not been characterized, and up to the present no adequate explanation for the jaundice has been put forward (D6). 

The urea cycle, also called ornithine cycle, was first described by H.A. Krebs and K. Henseleit in 1932. (quot. 51) The principle of ammonia detoxification in the urea cycle is based on the conversion of ammonium and bicarbonate in the mitochondria under ATP consumption into carbamoyl phosphate (by means of carbamoyl phosphate synthetase). It enters the urea cycle, which is localized mainly - yet with a low affinity for ammonium - in the periportal zone of the liver lobule. In the urea cycle alone, about two thirds of the amino nitrogen of ammonia are irretrievably lost to the organism (= definitive ammonia detoxification), (s. fig. 3.12)... 

In children and adults, signs of non-specific reactive hepatitis have also been observed. (42, 47) Acidophilic liver cell necrosis occasionally develops, depending on the type of red corpuscles. The endothelial cells are distended, the portal zones show inflammatory infiltration and granulomas or retothelial nodules are frequently found, (s. fig. 25.4) The pathogens can be demonstrated in the liver. Cirrhosis may develop, especially after the destruction of the lobular architecture as a sequela of extensive parenchymal necrosis. There are various serological tests available, including the Sabin-Feldmann... 

Plasmodium vivax, the cause of benign tertian malaria, produces milder clinical attacks than those of P. falciparum, and death is uncommon even in untreated cases. The build-up of immunity in the host rapidly controls the infection and schizonts disappear from the blood stream. The exo-erythro-cytic forms in the liver, unaffected by immunity, continue asexual division and reinvade the circulation when immunity has fallen once more these relapses are characteristic of vivax malaria and occur for at least two years after the primary infection. Infections due to P. ovale also follow a tertian pattern, but are much milder and more responsive to therapy than those due to P. vivax and relapses are less frequent. Infections due to both these parasites often display a prolonged incubation period between the primary infection and the development of malarial symptoms. P. vivax is widely distributed north and south of the equator, extending from the tropics to the temperate zones, while P. ovale is restricted to tropical Africa and the western Pacific. 

At doses of 2 g/kg or more, erosion zones in the stomach mucosa were observed with disappearance of the surface epithelium and hemorrhagic exudation of the muscula-ris mucosae. Swelling of cells in the liver was observed at doses over 1.5 g/kg. The no observed adverse effect level (NOAEL) was reported as 1 g/kg (Fandohan et al. 2008). 

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