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G Bories

Publications and source records attributed to G Bories.

25 records · Page 2Linked to original sources
PubMed1975

[Hydrocarbons of the spiruline algae: nature, metabolism of heptadecane by rats and swine].

Hydrocarbons represent about half of the insaponifiable fraction of spirulina algae (0.1 to 0.3 p. 100 of the dry alga); n-heptadecane is the major component (65 p. 100). The retention of this paraffin has been measured in animals receiving these algae as the main or partial protein source. Rats fed with a diet containing 280 ppm n-heptadecane (25 p. 100 alga meal) from weaning show an accumulation of this hydrocarbon in the carcass the retention levels off after 4 months and seems related to the lipid content; preferential fixation occurs in adipose tissue. Sows receiving a diet with 52 ppm heptadecane (5p. 100 alga meal) during growth, pregnancy and lactation retain comparatively much less hydrocarbon; nevertheless n-heptadecane is excreted in the milk.

Adipose Tissue↗
PubMed1975

[Determination of 3, 4-benzopyrene in spiruline algae produced and treated by various procedures].

Spirulina algae grow in highly salted natural lakes. Artificial cultivation in tanks with addition of carbon dioxide (natural gas, burned gases) has been studied in order to improve the biosynthesis. A possible 3, 4-benzopyrene (BaP) contamination must be then considered. Several BaP determinations have been performed in batches of algae from bath origins, prepared following different processes (filtration, spray, cylinder drying). BaP contents are very low (2 to 3 ppb) and comparable between batches.

Benzopyrenes↗
PubMedDate not supplied

Mercapturic acid conjugates as urinary end metabolites of the lipid peroxidation product 4-hydroxy-2-nonenal in the rat.

4-Hydroxy-2-nonenal (HNE), an aldehyde end product of lipid peroxidation in biological systems, is capable of producing a range of powerful biological effects. Despite its biological relevance, the metabolic fate of this aldehyde is unknown in vivo. This study examines the urinary excretion of HNE in the rat and the nature of metabolites formed. Following iv administration of [3H]HNE, the majority of the dose appeared in urine (67.1% after 48 h). The radio-HPLC metabolic profile showed that no unchanged parent compound was detected in urine whereas at least four metabolites were present, most of them corresponding to mercapturic acid conjugates. Two major pathways were involved in the biotransformation of HNE in vivo: (i) reduction/oxidation of the aldehyde group, and (ii) conjugation to endogenous glutathione leading to mercapturic acid conjugates in urine. These end products were isolated by HPLC and identified by mass spectrometry as HNE mercapturic acid, 1,4-dihydroxynonene mercapturic acid, 4-hydroxynonenoic mercapturic acid, and the corresponding lactone.

Acetylcysteine↗
PubMedDate not supplied

Chloramphenicol oxamylethanolamine as an end product of chloramphenicol metabolism in rat and humans: evidence for the formation of a phospholipid adduct.

Chloramphenicol (CP) has been implicated as, although not proven to be, a causative agent of aplastic anemia in humans. Recent studies from our laboratory have presented evidence that CP-oxamylethanolamine was an end product of CP biotransformation in birds. Because this novel metabolic pathway has never been reported in other species, we have now expanded these investigations to rat and humans. [3H]CP was administered po (10 mg/kg) to adult male Wistar rats and to a human volunteer. Urine was collected and analyzed by HPLC and GC-MS for CP metabolite determination. In rat, the two most important metabolites in 0-24 h urine were CP-base and CP-acetylarylamine which together accounted for about 50% of the ingested radioactivity. The remainder was due to unchanged CP, CP-oxamic acid, CP-alcohol, CP-glucuronide, and CP-oxamylethanolamine. The presence of these end products was also demonstrated in man. CP-oxamylethanolamine represented 0.74% and 1.37% of the ingested radioactivity in rat and human urine samples, respectively. CP-oxamylethanolamine formation was confirmed in vitro with isolated rat hepatocytes, suggesting the involvement of liver in the production of this metabolite. The origin of CP-oxamylethanolamine has been investigated with the use of hepatic liver microsomes from phenobarbital-treated rats. The incubation of [3H]CP with this subcellular fraction led to the binding of a radiolabeled compound to the microsomal lipids, whereas no binding occurred when CP-oxamic acid was incubated with the microsomes. Enzymatic hydrolysis of the microsome lipid fraction with phospholipase D from Streptomyces chromofuscus released CP-oxamylethanolamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

New aspects of metabolic conjugation of chloramphenicol.

New and major chloramphenicol (CP) metabolites have been isolated from the urine of goats administered [3H]CP. The CP-3-sulfoconjugate has been identified formally from its chromatographic behaviour and mass spectrometric analysis, as well as from incubations of CP with liver cytosol, using synthetic CP-conjugate as reference. Only a strong assumption is made of the identity of the CP-3-phosphoconjugate.

Animals↗
PubMedDate not supplied

Evidence for new metabolic pathways of chloramphenicol in the duck.

Following subcutaneous administration of [3H]chloramphenicol (CP) to duck, HPLC and TLC analyses showed that the two most important metabolites in 0- to 24-hr excreta were CP-oxamic acid and CP-alcohol, which together accounted for about one-third of the radioactivity therein. The remainder was due to unchanged CP (15% dose), CP-base (5% dose), and various metabolites representing < 4% dose each. Among these, CP-glucuronide and CP-sulfate have been previously isolated in mammals. In addition to these metabolites, several previously unreported in vivo CP biotransformation products were identified in this study by HPLC and MS comparison with synthetic reference compounds. These new metabolites were unequivocally identified as 1-O-monoacetyl CP, CP-1,3-diacetate, N-acetyl CP-base, CP-oxamylglycine, and CP-oxamylethanolamine. Besides these formally identified compounds, the CP-phosphate structure was tentatively assigned to a conjugate metabolite resistant to beta-glucuronidase and sulfatase hydrolysis. The possible origin of these metabolites is discussed extensively.

Animals↗