Induction by beta-bungarotoxin of apoptosis in cultured hippocampal neurons is mediated by Ca(2+)-dependent formation of reactive oxygen species.

The component of the venom of the Taiwanese banded krait Bungarus multicinctus, beta-bungarotoxin (beta-BuTx), acts as an extremely potent inducer of neuronal apoptosis when applied to rat hippocampal cultures. While induction of cell death is dependent on toxin binding to voltage-activated K+ channels and subsequent internalization, the pro-apoptotic signals triggered by picomolar concentrations of beta-BuTx are not understood. Following toxin binding, a dramatic increase in intracellular Ca2+ became detectable after 30 min, and in reactive oxygen species (ROS) after 3-4 h.

Beta-bungarotoxin is a potent inducer of apoptosis in cultured rat neurons by receptor-mediated internalization.

The neurotoxic phospholipase A(2), beta-bungarotoxin (beta-BuTx), is a component of the snake venom from the Taiwanese banded krait Bungarus multicinctus. beta-BuTx affects presynaptic nerve terminal function of the neuromuscular junction and induces widespread neuronal cell death throughout the mammalian and avian CNS. To analyse the initial events of beta-BuTx-mediated cell death, the toxin was applied to cultured rat hippocampal neurons where it induced neuronal cell death in a concentration-dependent manner (EC(50) approximately equal to 5 x 10(-13) M) within 24 h.

[Role of phospholipids in functionally different cell membranes under conditions of antioxidant system disturbance].

Vitamin E deficiency in organism leads to microsome membrane phospholipid composition changes, oxidation, superoxide dismutase (SOD) activity decrease, accompanied with the disorders of lung and liver tissues functional state which is connected with regulation of membrane penetration. The negative effect of E-hypovitaminosis more affects the liver than lung, which is caused by their different functional purposes, peculiarities of metabolic processes as well as by the content of biomembrane structural components. Vitamin E protects phospholipids from oxidation, regulates AOS condition, SOD-activity and promotes in such way the tissue functional disturbances correction of the animals tested.