Stannous chloride can disrupt neurological function by producing stimulation or depression. - GreenMedInfo Summary
Biological effects of stannous chloride, a substance that can produce stimulation or depression of the central nervous system.
Brain Res Bull. 2002 Nov 30;59(3):213-6. PMID: 12431751
Laboratorio de Radiofarmacia Experimental, Departamento de Biofisica e Biometria, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil.
It was demonstrated that tin, as stannous chloride (SnCl(2)), can facilitate the neuromuscular transmission by accelerating the transmitter release from the nerve terminals in the mouse. When this salt is injected into laboratory animals, it can produce stimulation or depression of the central nervous system. Because calcium (Ca(2+)) influx into the cytoplasm is indispensable to release the transmitter, it would be possible that SnCl(2) increases the Ca(2+) influx at the nerve terminals but not by blocking the K(+) channels. SnCl(2) is known to inhibit the immune response in rodents and to induce tumor generation in thyroid gland. There is no general agreement regarding its genotoxicity and it was discussed that the effects of this salt might depend on the physicochemical conditions and the route of its administration. SnCl(2) has been used in many sectors of human interest, such as food industry and nuclear medicine. This salt is directly administered to human beings endovenously, when it is used as a reducing agent to prepare 99mTc-radiopharmaceuticals which are also used for cerebral studies. SnCl(2) is capable to promote the generation of reactive oxygen species (ROS) that are responsible for the oxidative stress. Oxidative stress has been related with aging and other neurological diseases. So, it is relevant to evaluate other biological effects of SnCl(2). We decided to study these effects using Escherichia coli mutant strains, deficient in DNA repair genes, and supercoiled plasmid DNA. We evaluated the influence of medicinal plants, metal chelating agents, and ROS scavengers against the SnCl(2) deleterious effects. Our results show that SnCl(2) produced lesions in vitro as well as in vivo. This inactivation may be due to the production of ROS. We observed that the genotoxic effect of SnCl(2) was partly inhibited or disappeared, when the treatments were done in the presence of medicinal plants, metal chelating agents, and ROS scavengers. In conclusion, these findings suggest that the SnCl(2) biological effects may be associated with the generation of ROS. Moreover, we can speculate that ROS could be associated with the detrimental effects in the brain due to exogenous or endogenous metals.