Figure 1From: Project summary: a critical synopsis of mechanisms of action of low-dose xenobiotics in mammalian organisms as a basis for assessing aggregated effects of chemical mixtures and identifying "new" toxicological end pointsSchematic representation of the molecular mechanism of the neurotoxicity of type-2 alkenes. (A) Sulfhydryl-NO-controlled processes in neurotransmitter transport: 1. neurotransmitter storage in vesicles; 2. inflow of calcium for vesicle migration to presynaptic membrane and release of neurotransmitters; 3. uptake of neurotransmitters via post-synaptic membrane; 4. re-entry of excess neurotransmitters via presynaptic membrane. (B) Disturbance of pumping function by type-2 alkenes. The sulfhydryl-NO bond is physiologically reversible; to achieve this, pumps and channels are activated, opened and closed as needed (e.g. Ca2+-ion channel, above). Binding of type-2 alkenes is irreversible, so that control processes can no longer be modulated.Back to article page