No abstract

The administration of small amounts of mercuric compounds to pregnant rats, injected with 75Se in the form of selenite, markedly increased their retention of 75Se and simultaneously decreased the 75Se content in their foetuses. The 75Se concentration in the blood and liver of foetuses from these rats was much lower than in the blood and liver of foetuses from control mothers injected with [75Se]selenite only (or receiving zinc chloride instead ofmercuric chloride). Retention of 75Se in the maternal organs and the passage of 75Se into the foetuses was partially dependent on the dose of mercury. In the doses used in these experiments, administration of mercuric salts did not result in foetal death nor in any significant effect on the weight of the offspring. In lactating rats, the administration ofmercuric salts had a similar effect on the passage of 75Se into the milk. This resulted in a much smaller 75Se content in the newborn and suckling young of mothers exposed to small amounts of mercuric compounds during pregnancy or lactation than in control animals.

The paper considers the effects of bedaquiline (BDQ), an antituberculous preparation of the new generation, on rat liver mitochondria. It was shown that 50 μM BDQ inhibited mitochondrial respiration measured with substrates of complexes I and II (glutamate/malate and succinate/rotenone systems respectively) in the states V and V. At the same time, at concentrations below 50 μM, BDQ slightly stimulated respiration with substrates of complex I in the state V. BDQ was also found to suppress, in a dose-dependent manner, the activity of complex II and the total activity of complexes II + III of the mitochondrial transport chain. It was discovered that at concentrations up to 10 μM, BDQ inhibited HO production in mitochondria. BDQ (10-50 μM) suppressed the opening of Ca-dependent CsA-sensitive mitochondrial permeability transition pore. The latter was revealed experimentally as the inhibition of Ca/P-dependent swelling of mitochondria, suppression of cytochrome c release, and an increase in the Ca capacity of the organelles. BDQ also decreased the rate of mitochondrial energy-dependent K transport, which was evaluated by the energy-dependent swelling of mitochondria in a K buffer and DNP-induced K efflux from the organelles. The possible mechanisms of BDQ effect of rat liver mitochondria are discussed.

No abstract