Propionate metabolism

Metabolism of propanoate begins with its conversion to propionyl coenzyme A (propionyl-CoA), the usual first step in the metabolism of carboxylic acids. Since propanoic acid has three carbons, propionyl-CoA can directly enter neither beta oxidation nor the citric acid cycles. In most vertebrates, propionyl-CoA is carboxylated to D-methylmalonyl-CoA, which is isomerised to L-methylmalonyl-CoA. A vitamin B 12 -dependent enzyme catalyzes rearrangement of L-methylmalonyl-CoA to succinyl-CoA, which is an intermediate of the citric acid cycle and can be readily incorporated there.

No metabolites of fluticasone propionate were detected in an in vitro study of radiolabeled fluticasone propionate incubated in a human skin homogenate. The total blood clearance of systemically absorbed fluticasone propionate averages 1,093 mL/min (range, 618 to 1,702 mL/min) after a 1-mg intravenous dose, with renal clearance accounting for less than % of the total. Fluticasone propionate is metabolized in the liver by cytochrome P450 3A4-mediated hydrolysis of the 5- fluoromethyl carbothioate grouping. This transformation occurs in 1 metabolic step to produce the inactive17-ß-carboxylic acid metabolite, the only known metabolite detected in man. This metabolite has approximately 2,000 times less affinity than the parent drug for the glucocorticoid receptor of human lung cytosol in vitro and negligible pharmacological activity in animal studies. Other metabolites detected in vitro using cultured human hepatoma cells have not been detected in man.

Table 1. Oxidative pathways of glycolysis employed by various bacteria. Bacterium Embden-Meyerhof pathway Phosphoketolase (heterolactic) pathway Entner Doudoroff pathway Acetobacter aceti - + - Agrobacterium tumefaciens - - + Azotobacter vinelandii - - + Bacillus subtilis major minor - Escherichia coli + - - Lactobacillus acidophilus + - - Leuconostoc mesenteroides - + - Pseudomonas aeruginosa - - + Vibrio cholerae minor - major Zymomonas mobilis - - +

The normal inflammatory response to local infections can be masked by halobetasol. Application of topical corticosteroids to areas of infection, including tuberculosis of the skin, dermatologic fungal infection, and cutaneous or systemic viral infection (., measles or varicella), should be initiated or continued only if the appropriate antiinfective treatment is instituted. Herpes infection may be transmitted to other sites, including the eye. If the infection does not respond to the antimicrobial therapy, the concurrent use of the topical corticosteroid should be discontinued until the infection is controlled. Topical corticosteroids may delay the healing of non-infected wounds, such as venous stasis ulcers.

Propionate metabolism

propionate metabolism

The normal inflammatory response to local infections can be masked by halobetasol. Application of topical corticosteroids to areas of infection, including tuberculosis of the skin, dermatologic fungal infection, and cutaneous or systemic viral infection (., measles or varicella), should be initiated or continued only if the appropriate antiinfective treatment is instituted. Herpes infection may be transmitted to other sites, including the eye. If the infection does not respond to the antimicrobial therapy, the concurrent use of the topical corticosteroid should be discontinued until the infection is controlled. Topical corticosteroids may delay the healing of non-infected wounds, such as venous stasis ulcers.

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