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Korotkov SM, Glazunov VV, Yagodina OV.
J Biochem Mol Toxicol. 2007;21(2):81-91
Increase in the toxic effects of Tl+ on isolated
rat liver mitochondria in the presence of nonactin.
Sechenov Institute of Evolutionary Physiology and
Biochemistry, Russian Academy of Sciences, Thorez pr. 44, 194223
St. Petersburg, Russia.
The effects of Tl(+) ions on isolated rat liver
mitochondria were studied in the presence of nonactin, a cyclic
ionophore. Nonenergized rat liver mitochondria were increasingly
swollen at an elevated concentration of Tl(+) in the 160 mOsm
medium containing 0-150 mM sucrose and 0-75 mM TlNO(3) or 0-50
mM Tl acetate. On the contrary, mitochondria in experiments with
nonactin were contracted in the medium with 5-25 mM Tl(+) and
were swollen only in the medium with 50-75 mM TlNO(3) or 50 mM
Tl acetate. State 4 respiration along with swelling of
succinate-energized mitochondria followed contraction after
their deenergization was further enhanced at increasing
concentration of Tl acetate in a medium containing nonactin.
Regardless of the presence of nonactin, State 3 and
2,4-dinitrophenol (DNP)-stimulated respiration and the monoamine
oxidase (MAO) activity were not affected in the medium with 0-25
mM Tl acetate and sucrose. DNP-stimulated respiration decreased
and the MAO activity somewhat increased in the medium containing
50 mM Tl acetate and nonactin. Uptake of (86)Rb(+) by energized
mitochondria in the presence of valinomycin was considerably
decreased when Tl(+) and nonactin were simultaneously present in
the medium. An increase of the toxic effect of Tl(+) on rat
liver mitochondria in the presence of nonactin is accounted for
by disruption of mitochondria due to their more extensive
swelling and uncoupling of mitochondria, resulting in the
stimulation of State 4 and depletion of their energy store.
PMID: 17427175 |
