Pro-oxidative, genotoxic and cytotoxic properties of uranyl ions.

It is demonstrated that hydroxyl radicals and hydrogen peroxide are formed under the action of uranyl ions in aqueous solutions containing no reducing agents. In the presence of uranyl ions, formation of 8-oxoguanine in DNA and long-lived protein radicals are observed in vitro. It is shown that the pro-oxidant properties of uranyl at micromolar concentrations mostly result from the physico-chemical nature of the compound rather than its radioactive decay. Uranyl ions lead to damage in DNA and proteins causing death of HEp-2 cells by necrotic pathway. It is revealed that the uranyl ions enhance radiation-induced oxidative stress and significantly increase a death rate of mice exposed to sublethal doses of X-rays.

Peculiarities of the development of analgesic effect during transcutaneous dynamic electrical stimulation.

The effect of transcutaneous dynamic electrical neurostimulation on the development of analgesia was studied in behavioral and electrophysiological experiments on rats. A 30-min dynamic electrical stimulation elevated the nociception threshold in tail-flick and hot plate tests, increased the threshold of the late nociceptive flexor reflex, and decreased the number of bursts in the response. Intraperitoneal injection of naloxone (2 mg/kg) abolished the analgesic effect of dynamic electrical neurostimulation. It is concluded that the key role in reflex analgesia during dynamic electrical neurostimulation is played by the endogenous cerebral opioid system, which inhibits the nociceptive signals traveling to CNS via unmyelinated C-fiber afferents.

[Morphine does not prevent the development of a pain syndrome in rats induced by transection of the sciatic nerve]. / Morfin ne predotvrashchaet razvitie bolevogo sindroma u krys, vyzvannogo pererezkoi sedalishchnogo nerva.

The effects of morphine on the development of the neurogenic pain syndrome were studied in rats after sciatic nerve dissection. Morphine was injected subcutaneously in doses of 0.1, 1.0, and 5.0 mg/kg every day, starting on the first day after dissection. It has been shown that despite the fact that morphine initially arrests the development of the pain syndrome, then it intensifies its course. Possible mechanisms responsible for the inefficacy of morphine in neurogenic pain syndromes are discussed.