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Effects of Osmotic Pressure on the Oxidative Metabolism of Leishmania major Promastigotes
Author(s) -
BLUM J. JOSEPH
Publication year - 1991
Publication title -
the journal of protozoology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.067
H-Index - 77
eISSN - 1550-7408
pISSN - 0022-3921
DOI - 10.1111/j.1550-7408.1991.tb04434.x
Subject(s) - mannitol , osmotic shock , osmotic pressure , glycerol , osmotic concentration , chemistry , biochemistry , oxidative phosphorylation , alanine , oxidative stress , trehalose , osmoregulation , biology , amino acid , salinity , ecology , gene
Leishmania major promastigotes were washed and resuspended in an iso‐osmotic buffer. The rate of oxidation of 14 C‐labeled substrates was then measured as a function of osmolality. An acute decrease in osmolality (achieved by adding H 2 O to the cell suspension) caused an increase in the rates of 14 CO 2 production from [6‐ 14 C]glucose and, to a lesser extent, from [1, (3)‐ 14 C]glycerol. An acute increase in osmolality (achieved by adding NaCl, KCl, or mannitol) strongly inhibited the rates of 14 CO 2 production from [1‐: 14 C]alanine, [1‐ 14 C]glutamate, and [1, (3)‐ 14 C]glycerol. The rates of 14 CO 2 formation from [1‐ 14 C]laurate, [1‐ 14 C]acetate, and [2‐ 14 C]glucose (all of which form [1‐ 14 C]acetyl CoA prior to oxidation) were also inhibited, but less strongly, by increasing osmolality. These data suggest that with increasing osmolality there is an inhibition of mitochondrial oxidative capacity, which could facilitate the increase in alanine pool size that occurs in response to hyper‐osmotic stress. Similarly, an increase in oxidative capacity would help prevent a rebuild up of the alanine pool after its rapid loss to the medium in response to hypo‐osmotic stress.