d-Amino-acid oxidase is not present in the mouse liver

Konno, Ryuichi; Sato, Masato; Asakura, Setsuko; Fukui, Kiyoshi; Enami, Jumpei; Niwa, Akira

doi:10.1016/s0304-4165(96)00136-5

Cited by 34 publications

(30 citation statements)

References 49 publications

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“…and production of L-NNA than homogenates of the liver, which, in turn, has greater activity than homogenates of the brain, heart, lungs, and skeletal muscle. The activity of DAAO is highest in the kidneys followed by the liver and brain, in accordance with reports of greater expression of DAAO in the kidneys (Konno et al, 1997;Pilone, 2000;Hasegawa et al, 2004). Taken together, it is concluded that the renal DAAO plays an essential role in the chiral inversion of D-amino acids and accounts for approximately 80% D-NNA jpet.aspetjournals.org conversion in the body.…”

Section: Discussionsupporting

confidence: 89%

Renal d-Amino Acid Oxidase Mediates Chiral Inversion ofN^G-Nitro-d-arginine

Xin

Zhou²,

Cheng³

et al. 2004

J Pharmacol Exp Ther

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Section: Discussionsupporting

confidence: 89%

Renal d-Amino Acid Oxidase Mediates Chiral Inversion ofN^G-Nitro-d-arginine

Xin

Zhou²,

Cheng³

et al. 2004

J Pharmacol Exp Ther

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“…Additional support for this hypothesis is provided by the lack of hepatotoxicity of D-Met, which is a poor substrate for L-amino acid-specific transaminases. Transamination of D-Met can be accomplished by D-amino acid oxidase, but this enzyme is not present in mouse liver (Konno et al, 1997).…”

Section: Discussionmentioning

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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“…In context with the latter, the apparently species-specific DAAO accumulation in the renal cortex of rats with the exposure to propiverine and other compounds (Gopinath et al 1987;Hard and Snowden 1991;Dietrich et al 2008;Radi et al 2013;Shimoyama et al 2014) is reminiscent of the well-known species-and sex-specific accumulation of α2u-globulin in rats, also causally related to the exposure to numerous chemicals (Swenberg 1993). Contrary to α2u-globulin, which is synthesized in the liver of male rats under androgenic control and reabsorbed in the proximal tubules (Borghoff et al 1990), DAAO appears to be transcribed and translated in the proximal tubule proper (Konno et al 1997). Treatment of rats with propiverine did not increase renal proximal tubule rDAAO mRNA level (Heussner et al 2016), thus excluding increased gene expression as a potential explanation of the propiverine-mediated rDAAO accumulation.…”

Section: Discussionmentioning

confidence: 99%