Substrate-dependent cadmium toxicity affecting energy-linked K+/86Rb transport in Staphylococcus aureus.

Abstract:

:Bacteria accumulate high amounts of potassium in the cytoplasm. For studying transport of K+ (with 86Rb as a marker) in bacteria (Staphylococcus aureus 17810S), the cells were depleted of the internal K+ pool by a DNP treatment. Kinetics and energetics of 86Rb transport was assayed with glucose as an exogenous energy source. It was shown that 86Rb uptake proceeded via a low affinity K+ transport system with an apparent K(m) of 2.3 mmol/L Rb+. Studies with the lipophilic cation TPP+ (tetraphenylphosphonium), the protonophore CCCP (carbonyl cyanide 3-chlorophenylhydrazone) and inhibitors (HQNO--2-heptyl-4-hydroxyquinoline N-oxide; iodoacetate) indicated that 86Rb transport was driven by delta psi (membrane potential) generated via the respiratory chain. The effect of Cd2+ on 86Rb transport was assayed with two energy donors--glucose and L-lactate. It was found that Cd2+ strongly inhibited delta psi-dependent 86Rb transport energized by cadmium-sensitive glucose oxidation, but was not toxic when cadmium-insensitive L-lactate was used as an energy source. The mechanism of these differential, substrate-dependent effects of Cd2+ on 86Rb transport is discussed.

journal_title

Folia microbiologica

authors

Tynecka Z,Malm A,Kosikowska U,Kot A

doi

10.1007/BF02816378

keywords:

subject

Has Abstract

pub_date

1998-01-01 00:00:00

pages

617-22

issue

6

eissn

0015-5632

issn

1874-9356

journal_volume

43

pub_type

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