Effect of biotin, pantothenic acid and nicotinic acid deficiencies on amino acid transport in Lactobacillus plantarum

Abstract

1. 1.The effects of biotin, pantothenic acid, nicotinic acid and folic acid deficiencies and of physiological age on the rate and amount of glutamic acid accumulation in Lactobacillus plantarum have been investigated. 2. 2.The time-course of glutamic acid uptake was markedly affected by biotin and pantothenic acid deficiencies. After several minutes of uptake at a normal rate, accumulation ceased or continued slowly for 20 to 40 min, after which it resumed at a more rapid though generally inferior rate resulting in submaximal pool levels. 3. 3.High concentrations of sucrose restored uptake by these cells to a normal level and pattern. Acetate and the respective vitamin individually stimulated uptake by biotin and pantothenate-deficient cells and together they allowed normal uptake. With biotin-deficient cells, the stimulatory effect of biotin, but not of acetate, was inhibited slightly by chloramphenicol. With pantothenic acid-deficient cells high concentrations of KCl in contrast to sucrose failed to restore uptake to fully normal levels. 4. 4.In contrast, nicotinic acid-deficient cells accumulated glutamate and glycolyzed at markedly reduced rates. Sucrose and acetate failed to stimulate uptake, while nicotinic acid greatly improved the accumulation rate. The effects of this deficiency on uptake appear to be related primarily to energy metabolism. 5. 5.Early exponential phase, nutritionally normal cells also showed a slight dip in the accumulation curve which could be corrected by acetate and usually, although not consistently, by sucrose. Folic acid-limited cells accumulated as well as early exponential phase control cells indicating that this deficiency does not create any disturbance in the transport system. 6. 6.Penicillin inhibited amino acid uptake by early exponential phase cells much more than by early stationary phase cells and sucrose protected against this inhibition. 7. 7.The adverse effects of biotin and pantothenic acid deficiencies on amino acid transport may arise from structural changes in the cell. The reversal of these effects by high extracellular osmotic pressure indicates that these vitamins probably do not participate directly in the transport step. These findings are discussed in terms of the probable effects of biotin and pantothenate deficiencies on lipid synthesis and consequently on cell membrane structure. The facile reversal by osmotic means of the effects of these presumed membrane changes on transport suggests that membrane permeability properties and the activity of transport catalysts may not be strictly dependent on a specific membrane composition. An alternate possibility also is considered, viz., that the aberrations in accumulation activity occur primarily as a result of cell wall changes.