The induction of a specific form of cytochrome P-450 (P-450j) by fasting

Hong, Jun-Yan; Pan, Jingshun; Gonzalez, Frank J.; Gelboin, Harry V.; Yang, Chung S.

doi:10.1016/0006-291x(87)91525-7

Cited by 204 publications

(73 citation statements)

References 13 publications

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“…An earlier study did not observe any effect even with a 3-day fasting (Nakajima and Sato 1979), and another study found a significant increase of CYP until 3-day of starvation (Imaoka et al 1990). For the hepatic CYP2E1 content, some studies have shown the significant increase after one-day fasting (Hong et al 1987;Imaoka et al 1990). We further demonstrated that CYP2E1 increased significantly not only in the fasted rats but also in the rats consumed 15 kcal of food.…”

Section: Discussionmentioning

confidence: 99%

“…It is well-known that fasting potentiates the hepatotoxicity of chemicals, such as carbon tetrachloride (CCl 4 ), which is metabolically activated by cytochrome P450 (CYP) in hepatic microsomes (Hong et al 1987;Imaoka et al 1990;Ueng et al 1993;Wang et al 1995;Sheweita et al 2001). CYP2E1 is the most important isoform enhanced by fasting (Hong et al 1987;Imaoka et al 1990). Although fasting is very rare, dietary restriction (DR) is more common due to health reasons in developed countries or for economic reasons in some developing countries, or simply as a method of dieting for esthetic reasons.…”

Section: Measurements Of Hepatic Glutathione (Gsh) Content Microsomamentioning

confidence: 99%

“…In previous studies, researchers have always observed the effects of the duration of fasting (from 12-hr to 72-hr) on the hepatic metabolism and hepatotoxicity (Nakajima et al 1982;Hong et al 1987;Imaoka et al 1990;Ueng et al 1993;Wang et al 1995). To our knowledge, there have been no reports that have designated the amount of food intake at five levels including conventional feeding (60 kcal), three of DR (45, 30 and 15 kcal) and fasting (0 kcal).…”

Section: Measurements Of Hepatic Glutathione (Gsh) Content Microsomamentioning

confidence: 99%

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One-Day Dietary Restriction Changes Hepatic Metabolism and Potentiates the Hepatotoxicity of Carbon Tetrachloride and Chloroform in Rats

Qin

Wang

et al. 2007

Tohoku J. Exp. Med.

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Although dietary restriction (DR) is common in modern society, research about hepatic metabolism and the hepatotoxicity induced by DR has been conducted less intensively than that induced by fasting. In the present study, we fed male Wistar rats at five levels of food intake for one day, including conventional feeding (60 kcal), three of DR (45, 30, and 15 kcal), and fasting (0 kcal), and observed the metabolic changes of hepatic cytochrome P450 2E1(CYP2E1) and the hepatotoxicity of chloroform (CHCl 3 ) and carbon tetrachloride (CCl 4 ). The CYP2E1 content was significantly increased in 15 kcalfood and fasting groups. The hepatic glutathione (GSH) content, which protects the liver from hepatotoxic agents, was depleted in 15 kcal-food and fasting groups. After the challenge by CHCl 3 and CCl 4 , the activities of aspartate aminotransferase and alanine aminotransferase, marker enzymes for liver damage, were elevated remarkably at all food groups. Moreover, their activities increased significantly in DR groups, in comparison to the corresponding 60 kcal-food group. After the challenge, the hepatic GSH content was also depleted significantly in 15 kcal-food and fasting groups. CHCl 3 was cleared by hepatic metabolism about 8-10 times faster than that of CCl 4 . Similarly, the areas under the blood concentration-time curve of CCl 4 was as much as twice that of the corresponding CHCl 3 . In conclusion, when food was restricted to less than half of conventional amount, hepatic metabolism was affected and the hepatotoxicity induced by CCl 4 or CHCl 3 was augmented by, at least in part, CYP2E1 induction and GSH depletion. dietary restriction; hepatotoxicity; hepatic cytochrome P450 2E1; chloroform; carbon tetrachloride

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Section: Discussionmentioning

confidence: 99%

Section: Measurements Of Hepatic Glutathione (Gsh) Content Microsomamentioning

confidence: 99%

Section: Measurements Of Hepatic Glutathione (Gsh) Content Microsomamentioning

confidence: 99%

See 1 more Smart Citation

One-Day Dietary Restriction Changes Hepatic Metabolism and Potentiates the Hepatotoxicity of Carbon Tetrachloride and Chloroform in Rats

Qin

Wang

et al. 2007

Tohoku J. Exp. Med.

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“…For example, CYP2E1 levels were elevated in chronically obese, overfed rats and in rats fed a highfat diet (84). Somewhat paradoxical, in rats levels of CYP2E1 were increased by fasting and by prolonged starvation (85,86). Diabetes has been reported to increase the expression of CYP2E1 mRNA and protein levels several fold (87).…”

Section: Induction and Regulation Of Cyp2e1mentioning

confidence: 99%

CYP2E1 and oxidative liver injury by alcohol

Cederbaum

2008

Free Radical Biology and Medicine

651

534

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Ethanol-induced oxidative stress appears to play a major role in mechanisms by which ethanol causes liver injury. Many pathways have been suggested to contribute to the ability of ethanol to induce a state of oxidative stress. One central pathway appears to be the induction of cytochrome P450 2E1 (CYP2E1) by ethanol. CYP2E1 metabolizes and activates many toxicological substrates, including ethanol, to more reactive, toxic products. Levels of CYP2E1 are elevated under a variety of physiological and pathophysiological conditions, and after acute and chronic alcohol treatment. CYP2E1 is also an effective generator of reactive oxygen species such as the superoxide anion radical and hydrogen peroxide, and in the presence of iron catalysts, produces powerful oxidants such as the hydroxyl radical. This Review Article summarizes some of the biochemical and toxicological properties of CYP2E1, and briefly describes the use of cell lines developed to constitutively express CYP2E1 in assessing the actions of CYP2E1. Possible therapeutic implications for treatment of alcoholic liver injury by inhibition of CYP2E1 or CYP2E1-dependent oxidative stress will be discussed, followed by some future directions which may help to understand the actions of CYP2E1 and its role in alcoholic liver injury.

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“…Effectively, activation of kinase can phosphorylate CYP, resulting in its inactivation (Rhee, 1999). CYP2E1 is significant for its adaptive response to high blood ethanol level, with a corresponding acceleration of ethanol metabolism, and is inducible by small organic molecules and pathophysiological states (Hong et al, 1987). However, the 80% suppression of CYP2E1 mRNA caused by the injection of endotoxin has also been reported (Morgan, 1993).…”

Section: Discussionmentioning

confidence: 99%

Effects of Trolox on the activity and gene expression of cytochrome P450 in hepatic ischemia/reperfusion

Eum

Lee

2004

British J Pharmacology

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1 The aim of this study was to investigate the effect of Trolox on hepatic microsomal cytochrome P450 (CYP) activity and gene expression during ischemia and reperfusion (I/R). 2 Rats were subjected to 60 min of hepatic ischemia, and 5 h (acute phase) and 24 h (subacute phase) of reperfusion. Rats were treated intravenously with Trolox (2.5 mg kg À1 ) or vehicle, 5 min before reperfusion. 3 The serum alanine aminotransferase level and lipid peroxidation were increased as a result of I/R. These increases were attenuated by Trolox. Reduced glutathione concentration decreased in I/R group, and this decrease was inhibited by Trolox. 4 Both total hepatic CYP content and NADPH-cytochrome P450 reductase activity decreased after I/R, which were restored by Trolox. 5 CYP1A1 activity and its protein level decreased 24 h after reperfusion; decreases which were prevented by Trolox. Both the activity and mRNA expression of CYP1A2 decreased 24 h after reperfusion. The decrease in CYP1A2 mRNA was prevented by Trolox. CYP2B1 activity and mRNA expression decreased 5 h after reperfusion. The decrease in CYP2B1 activity was prevented by Trolox. In contrast, the CYP2E1 activity and its protein level increased 5 h after reperfusion and this increase was prevented by Trolox. 6 The expression of TNF-a and iNOS mRNAs increased after I/R. Trolox inhibited increase in iNOS mRNA expression. 7 Trolox ameliorates hepatic drug-metabolizing dysfunction, as indicated by abnormalities in CYP isoforms during I/R, and this protection is likely due to the scavenging of reactive oxygen species.

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The induction of a specific form of cytochrome P-450 (P-450j) by fasting

Cited by 204 publications

References 13 publications

One-Day Dietary Restriction Changes Hepatic Metabolism and Potentiates the Hepatotoxicity of Carbon Tetrachloride and Chloroform in Rats

One-Day Dietary Restriction Changes Hepatic Metabolism and Potentiates the Hepatotoxicity of Carbon Tetrachloride and Chloroform in Rats

CYP2E1 and oxidative liver injury by alcohol

Effects of Trolox on the activity and gene expression of cytochrome P450 in hepatic ischemia/reperfusion

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