Methionine transamination <i>in vivo</i>

Cooper, Arthur J. L.

doi:10.1042/bj2620689

Cited by 13 publications

(5 citation statements)

References 9 publications

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“…We have measured methionine transamination and glutamine transaminase K and L activity in skeletal muscles from rats and chicks (Table 1). Our results are not consistent with Cooper's theoretical concept that low glutamine transaminase activity in skeletal muscle may favour methionine degradation via a transamination pathway [1]. Although methionine is extensively transaminated in intact chick skeletal muscle incubated in the presence of 0.2-0.5 mM-methionine but in the absence of other amino acids [2], glutamine transaminase K and L activities are only barely detected in this tissue (Table 1).…”

contrasting

confidence: 98%

Methionine transamination and glutamine transaminases in skeletal muscle

Thompson

1989

Biochemical Journal

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contrasting

confidence: 98%

Methionine transamination and glutamine transaminases in skeletal muscle

Thompson

1989

Biochemical Journal

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“…1). Met TA is catalyzed by multiple transaminases including glutamine transaminase K and L and results in the formation of 2-keto-4-methylthiobutyric acid (Cooper, 1989;Scislowski and Pickard, 1993). 2-Keto-4-methylthiobutyric acid is then oxidatively decarboxylated by branched chain 2-oxo acid dehydrogenase complex to form 3-methylthiopropionic acid (3-MTP) Jones and Yeaman, 1986).…”

mentioning

confidence: 99%

l-Methionine Toxicity in Freshly Isolated Mouse Hepatocytes Is Gender-Dependent and Mediated in Part by Transamination

Dever¹,

Elfarra²

2008

J Pharmacol Exp Ther

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L-Methionine (Met) has been implicated in parenteral nutritionassociated cholestasis in infants and, at high levels, it causes liver toxicity by mechanisms that are not clear. In this study, Met toxicity was characterized in freshly isolated male and female mouse hepatocytes incubated with 5 to 30 mM Met for 0 to 5 h. In male hepatocytes, 20 mM Met was cytotoxic at 4 h as indicated by trypan blue exclusion and lactate dehydrogenase leakage assays. Cytotoxicity was preceded by reduced glutathione (GSH) depletion at 3 h without glutathione disulfide formation. Exposure to 30 mM Met resulted in increased cytotoxicity and GSH depletion. It is interesting to note that female hepatocytes were resistant to Met-induced cytotoxicity at these concentrations and showed increased cellular GSH levels compared with hepatocytes exposed to medium alone. The effects of amino-oxyacetic acid (AOAA), an inhibitor of Met transamination, and 3-deazaadenosine (3-DA), an inhibitor of the Met transmethylation pathway enzyme S-adenosylhomocysteine hydrolase, on Met toxicity in male hepatocytes were then examined. Addition of 0.2 mM AOAA partially blocked Met-induced GSH depletion and cytotoxicity, whereas 0.1 mM 3-DA potentiated Met-induced toxicity. Exposure of male hepatocytes to 0.3 mM 3-methylthiopropionic acid (3-MTP), a known Met transamination metabolite, resulted in cytotoxicity and cellular GSH depletion similar to that observed with 30 mM Met, whereas incubations with D-methionine resulted in no toxicity. Female hepatocytes were less sensitive to 3-MTP toxicity than males, which may partially explain their resistance to Met toxicity. Taken together, these results suggest that Met transamination and not transmethylation plays a major role in Met toxicity in male mouse hepatocytes.

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“…However, the link between Hcy and Hcy thiolactone in Met-induced liver toxicity has yet to be demonstrated. Met transamination produces 2-keto-4-methylthiobutyric acid (KMB) ( 44 , 45 ), which is then oxidatively decarboxylated to form 3-methylthiopropionic acid (3-MTP) ( 46 , 47 ). 3-MTP is further converted into highly toxic and volatile molecules such as methanethiol, hydrogen sulfide, and dimethylsulfide ( 46 , 48 – 50 ).…”

Section: Hypermethioninemia-induced Liver Damagementioning

confidence: 99%

Pathological role of methionine in the initiation and progression of biliary atresia

Jiachen,

Paul Kwong Hang,

Kenneth Kak Yuen

et al. 2023

Front. Pediatr.

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Methionine (Met) is an essential amino acid, and its excessive dietary intake and/or its metabolism disturbance could lead to accumulation/depletion of hepatic Met and some of the key intermediates of these pathways, which would interfere normal liver function and would be associated with liver diseases. Biliary atresia (BA) is a life-threatening disease characterized by inflammatory fibrosclerosing changes of the intrahepatic and extrahepatic biliary systems and is the primary cause of obstructive neonatal cholestasis with a rapid course of liver failure. However, its pathogenesis remains unknown. Previous studies reported elevated Met level in patients with obstructive cholestasis, suggesting a potential link between Met and BA. This paper reviews the Met metabolism in normal conditions and its dysregulation under abnormal conditions, the possible causes of hypermethioninemia, and its connection to BA pathogenesis: Abnormal hepatic level of Met could lead to a perturbation of redox homeostasis and mitochondrial functions of hepatocytes, enhancement of viral infectivity, and dysregulation of innate and adaptative immune cells in response to infection/damage of the liver contributing to the initiation/progression of BA.

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Methionine transamination in vivo

Cited by 13 publications

References 9 publications

Methionine transamination and glutamine transaminases in skeletal muscle

Methionine transamination and glutamine transaminases in skeletal muscle

l-Methionine Toxicity in Freshly Isolated Mouse Hepatocytes Is Gender-Dependent and Mediated in Part by Transamination

Pathological role of methionine in the initiation and progression of biliary atresia

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