Disease relevance of trimethylammonioboron

• 5. Relaxation to hypoxia or metabolic inhibition was unaffected when the change in pHi was neutralized by addition of the weak base trimethylamine (TMA) [1].
• A high cell concentration of more than 10(8) cfu/g of Shewanella putrefaciens is required for production of a TMA level normally found in spoiled fish [2].
• Intraperitoneal injections (daily from d 1 to 17 of gestation) of TMA at 2.5 and 5 mmol/kg/d significantly (p less than .001) decreased fetal body weight but not the placental weight or maternal body weight gain; however, 5 of 11 mice treated with 5 mmol/kg TMA died [3].

Psychiatry related information on trimethylammonioboron

• Although Alzheimer's patients, as a group, did not differ from controls with regard to probabilistic learning capacity (PLC), male AD patients, as compared to male controls, displayed an impairment in the task performance by 28% (P<0.03) and showed a 16% elevation in TMA signaling (P<0.04) [4].

High impact information on trimethylammonioboron

• TMA oxidation is catalyzed by flavin-containing mono-oxygenase (FMO; refs 7,8), and tissue localization and functional studies have established FMO3 as the form most likely to be defective in fish-odour syndrome [5].
• A fishy off-flavor is occasionally observed in cow's milk and it has been established recently that this phenotype is due to elevated TMA levels [6].
• We observed that in patients a high TMA signal in the basal ganglia region was correlated with a poorer performance in the probabilistic learning task (Spearman rank order correlation (SROC)=-0.6, P<0.009) [4].
• The only nonsynonymous mutation identified in the chicken FMO3 gene (T329S) changes an evolutionarily highly conserved amino acid and is associated with elevated levels of TMA and fishy taint in the egg yolk in several chicken lines [7].
• Addition of trimethylamine (Trima+, 20 mmol/l) alkalinized cytosolic pH (n=7) [8].

Biological context of trimethylammonioboron

• Confocal measurements of cell volume showed no significant changes induced by TriMA or acetate [9].
• Inhibition by TMA is indicative of a role for FMO in osmoregulation, catalysing the conversion of TMA to TMA N-oxide [10].
• [14C]Trimethylamine (TMA) was also used to investigate the possible role of trimethylamine oxide (TMAO) as an osmoregulatory compound in migrating prespawning cannulated Pacific pink salmon (Oncorhynchus gorbuscha) taken from marine or fresh water environments [11].
• Children with congenital disorders of energy metabolism had NAA/TMA ratios ranging from severely decreased to normal, but 7 of the 9 had high Lac signals, even in brains with normal NAA/TMA [12].

Anatomical context of trimethylammonioboron

• Methimazole oxidase activity was also observed in dogfish liver microsomes which was inhibited by trimethylamine (TMA) [13].

Associations of trimethylammonioboron with other chemical compounds

• The major FMO in adult human liver, FMO3, is responsible for trimethylamine (TMA) N-oxygenation [14].
• Flavin-containing mono-oxygenase 3 (FMO3) catalyses TMA oxidation and mutations in the FMO3 gene have recently been shown to underlie trimethylaminuria/fish odour syndrome [15].
• In the liver, this protein catalyzes the NADPH-dependent oxidative metabolism of odorous trimethylamine (TMA), derived in the gut from dietary sources, to nonodorous trimethylamine N-oxide (TMA N-oxide) [16].

Analytical, diagnostic and therapeutic context of trimethylammonioboron

• Intraperitoneal injections of TMA failed to induce activity [17].

References