ubiquinone and Drug-Hypersensitivity

Thiol hypersensitivity in a mutant of Escherichia coli (IS16) was reversed by complementation with a plasmid that carried the ubiX gene. The mutant had low ubiquinone content. Complementation elevated the ubiquinone level and eliminated thiol hypersensitivity. Analysis of chromosomal ubiX genes indicated that both parent and mutant strains were ubiX mutants. The low ubiquinone content of IS16 was possibly caused by a ubiD ubiX genotype. A ubiA mutant also exhibited thiol hypersensitivity. Neither IS16 nor the ubiA mutant strain could produce alkaline phosphatase (in contrast to their parent strains) after 2 h of induction, thus showing Dsb- phenotypes. The phenomena of thiol hypersensitivity and low ubiquinone content may be linked by their connections to the periplasmic disulfide bond redox machinery.

Topics: Amino Acid Sequence; Bacterial Proteins; Base Sequence; Carboxy-Lyases; Drug Hypersensitivity; Escherichia coli; Escherichia coli Proteins; Genetic Complementation Test; Molecular Sequence Data; Sulfhydryl Compounds; Ubiquinone

Topics: Adult; Bromazepam; Desensitization, Immunologic; Drug Hypersensitivity; Drug Therapy, Combination; Female; GABA Modulators; Humans; Kearns-Sayre Syndrome; Patch Tests; Skin Tests; Ubiquinone; Urticaria