Short-term beef consumption promotes systemic oxidative stress, TMAO formation and inflammation in rats, and dietary fat content modulates these effects.

A high consumption of red and/or processed meat is associated with a higher risk to develop several chronic diseases in which oxidative stress, trimethylamine-N-oxide (TMAO) and/or inflammation are involved. We aimed to elucidate the effect of white (chicken) vs. red (beef) meat consumption in a low vs. high dietary fat context (2 × 2 factorial design) on oxidative stress, TMAO and inflammation in Sprague-Dawley rats. Higher malondialdehyde (MDA) concentrations were found in gastrointestinal contents (up to 96% higher) and colonic tissues (+8.8%) of rats fed the beef diets (all P < 0.05). The lean beef diet resulted in lower blood glutathione, higher urinary excretion of the major 4-hydroxy-nonenal metabolite, and higher plasma C-reactive protein, compared to the other dietary treatments (all P < 0.05). Rats on the fat beef diet had higher renal MDA (+24.4% compared to all other diets) and heart MDA (+12.9% compared to lean chicken) and lower liver vitamin E (-26.2% compared to lean chicken) (all P < 0.05). Rats on the fat diets had lower plasma vitamin E (-23.8%), lower brain MDA (-6.8%) and higher plasma superoxide dismutase activity (+38.6%), higher blood glutathione (+16.9%) (all P < 0.05) and tendency to higher ventral prostate MDA (+14.5%, P = 0.078) and prostate weight (+18.9%, P = 0.073), compared to rats on the lean diets. Consumption of the beef diets resulted in higher urinary trimethylamine (4.5-fold) and TMAO (3.7-fold) concentrations (P < 0.001), compared to the chicken diets. In conclusion, consumption of a high beef diet may stimulate gastrointestinal and/or systemic oxidative stress, TMAO formation and inflammation, depending on the dietary fat content and composition.

Formation of cyclic enol ethers from a labile biological precursor: an example of analytical artifacts.

Three isomeric enol ethers are among those constituents apparently unique to mouse urine as identified by gas chromatographic analysis. These compounds appear to be artifacts arising from the cyclization and dehydration of 6-hydroxy-6-methyl-3-heptanone. Identification of the trimethylsilyl ether of 6-hydroxy-6-methyl-3-heptanone in the silylated ether extract of mouse urine indicates that the precursor keto alcohol is indeed present in the urine. Since similar heterocyclic compounds are often identified in urine samples analyzed by gas chromatography, formation of various analysis artifacts arising from analogous cyclization and dehydration reactions is likely.

Identification of 10, 11-epoxide and other cyclobenzaprine metabolites isolated from rat urine.

Cyclobenzaprine (40 mg/kg ip) was administered to rats, and six urinary metabolites of this drug were identified. They were the 10, 11-epoxide, the N -oxide, the desmethyl derivative, the hydroxylated and desmethylhydroxylated compounds, and the N-oxide hydroxylated at the 10- or 11-position. Mass spectrometric analysis confirmed their structures.

Epoxide metabolites of protriptyline in rat urine.

Two epoxide metabolites of 5-(3-methylaminopropyl)-5H-dibenzo[a,d]cycloheptene (protriptyline) were identified in the urine of rats given 14-C-labeled drug. They were characterized by mass spectrometry, nuclear magnetic resonance spectrometry, and chemical reactivity as 10,11-dihydro-10,11-epoxy-5(3-methylaminopropyl)-5H-dibenzo[a,d]cycloheptene (I) and 10,11-dihydro-10,11-epoxy-5(3-aminopropyl)-5H-dibenzo[a,d]cycloheptene (II). Over twice as much I as II was excreted and together the two metabolites accounted for approximately 40% of the urinary radioactivity.