Evidence for impairment of transsulfuration pathway in cirrhosis

Horowitz, Jed H.; Rypins, Eric B.; Henderson, J. Michael; Heymsfield, Steven B.; Moffitt, Steven D.; Bain, Raymond P.; Chawla, Rajender K.; Bleier, Julia C.; Rudman, Daniel

doi:10.1016/0016-5085(81)90489-3

Cited by 216 publications

(65 citation statements)

References 14 publications

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“…In these individuals, even small amounts of alcohol which have almost no effect on Caucasians can produce a rapid facial flush, frequently associated with tachycardia, headache and nausea [7]. This propensity for flushing is genetically determined and caused by decreased disposition secondary to the lack of ALDH2 activity [8][9][10][11]. In fact, the flushing reaction seen in susceptible Asians mimics to a lesser degree the disulfiram reaction caused by the elevation of acetaldehyde following aldehyde dehydrogenase inhibition.…”

Section: Role Of Acetaldehyde Dehydrogenasementioning

confidence: 98%

CYP2E1: from ASH to NASH

Lieber¹

2004

Hepatology Research

145

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Section: Role Of Acetaldehyde Dehydrogenasementioning

confidence: 98%

CYP2E1: from ASH to NASH

Lieber¹

2004

Hepatology Research

145

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“…Our laboratory was the first to identify hepatic deficiency of SAM in ALD in the early 1980s (Chawla et al, 1984;Horowitz et al, 1981). We observed that alcoholic subjects had a delayed clearance of an oral bolus of methionine but had no detectable accumulation of any metabolic intermediates of the transsulfuration pathway.…”

Section: Sam Affects Tnf-␣ Gene Expression In Macrophagesmentioning

confidence: 89%

“…Several studies implicate nutritional abnormalities as well as oxidative stress, free radical generation, lipid peroxidation, increased cytokine production, metabolic abnormalities, acetaldehyde-adduct formation, and impaired immunological response as major causes for alcoholic liver injury. Abnormal metabolism of SAM is an acquired metabolic abnormality in ALD that was first identified in our laboratory (Chawla et al, 1984;Horowitz et al, 1981) SAM is an obligatory intermediate in the transsulfuration pathway, a major pathway for the conversion of methionine to cysteine. The pathway, in its entirety, is localized in the liver, but major parts of this pathway exist in the brain, kidney, spleen, and several other tissues.…”

Section: Sam Affects Tnf-␣ Gene Expression In Macrophagesmentioning

confidence: 99%

How Is the Liver Primed or Sensitized for Alcoholic Liver Disease?

Tsukamoto

Takei

McClain

et al. 2001

Alcoholism Clin & Exp Res

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This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Hidekazu Tsukamoto and Yoshiyuki Takei. The presentations were (1) Tribute to Professor Rajendar K. Chawla, by Craig J. McClain; (2) Dysregulated TNF signaling in alcoholic liver disease, by Craig J. McClain, S. Joshi‐Barve, D. Hill, J Schmidt, I. Deaciuc, and S. Barve; (3) The role of mitochondria in ethanol‐mediated sensitization of the liver, by Anna Colell, Carmen Garcia‐Ruiz, Neil Kaplowitz, and Jose C. Fernandez‐Checa; (4) A peroxisome proliferator (bezafibrate) can prevent superoxide anion release into hepatic sinusoid after acute ethanol administration, by Hirokazu Yokoyama, Yukishige Okamura, Yuji Nakamura, and Hiromasa Ishii; (5) S‐adenosylmethionine affects tumor necrosis factor‐α gene expression in macrophages, by Rajendar K. Chawla, S. Barve, S. Joshi‐Barve, W. Watson, W. Nelson, and C. McClain; (6) Iron, retinoic acid and hepatic macrophage TNFα gene expression in ALD, by Hidekazu Tsukamoto, Min Lin, Mitsuru Ohata, and Kenta Motomura; and (7) Role of Kupffer cells and gut‐derived endotoxin in alcoholic liver injury, by N. Enomoto, K. Ikejima, T. Kitamura, H. Oide, Y. Takei, M. Hirose, B. U. Bradford, C. A. Rivera, H. Kono, S. Peter, S. Yamashina, A. Konno, M. Ishikawa, H. Shimizu, N. Sato, and R. Thurman.

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“…These results suggest that methionine transsulfuration (2) and cysteine oxidation (43) are confined to the liver, whereas transamination of cysteine (and methionine) is also occurring in extrahepatic tissues, such as skeletal muscle (1 1-13). The metabolic consequences of preserved sulfur amino acid transamination in patients with advanced forms of liver dysfunction is at present unclear, but recent studies suggest that some of these metabolites are toxic (3,7,9,53,54) and may have etiologic significance in the development of hepatic coma (9). Thus, sulfur amino acid metabolism must be carefully monitored in patients with advanced forms of liver disease, especially during nutritional supplementation with these compounds (3, 4, 10, 13, 55).…”

Section: J Mdrtensson Et Almentioning

confidence: 98%

Sulfur Amino Acid Metabolism in Hepatobiliary Disorders

Mårtensson¹,

Foberg²,

Frydén

et al. 1992

Scandinavian Journal of Gastroenterology

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Sulfur amino acid metabolism was studied in patients with mild to severe forms of liver dysfunction and compared with that of healthy controls. Patients with mild liver dysfunction (for example, Gilbert's syndrome) had a normal sulfur amino acid metabolism. With increased inflammatory activity and cirrhosis (for example, chronic active hepatitis, alcohol-induced cirrhosis, and hepatic coma) a decreased ability to metabolize methionine (to cysteine, with cystathionine accumulation) and cysteine (to inorganic sulfate, with thiosulfate and N-acetylcysteine accumulation) was found. In contrast, transaminative metabolism of sulfur amino acids was preserved in patients with advanced forms of liver dysfunction, suggesting that transamination of sulfur amino acids is performed not only in the liver but also in extrahepatic tissues. Some implications of these findings are discussed.

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Evidence for impairment of transsulfuration pathway in cirrhosis

Cited by 216 publications

References 14 publications

CYP2E1: from ASH to NASH

CYP2E1: from ASH to NASH

How Is the Liver Primed or Sensitized for Alcoholic Liver Disease?

Sulfur Amino Acid Metabolism in Hepatobiliary Disorders

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