Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 Jan 8;8:366.
doi: 10.3389/fendo.2017.00366. eCollection 2017.

Organotins in Neuronal Damage, Brain Function, and Behavior: A Short Review

Affiliations
Free PMC article
Review

Organotins in Neuronal Damage, Brain Function, and Behavior: A Short Review

Igor Ferraz da Silva et al. Front Endocrinol (Lausanne). .
Free PMC article

Abstract

The consequences of exposure to environmental contaminants have shown significant effects on brain function and behavior in different experimental models. The endocrine-disrupting chemicals (EDC) present various classes of pollutants with potential neurotoxic actions, such as organotins (OTs). OTs have received special attention due to their toxic effects on the central nervous system, leading to abnormal mammalian neuroendocrine axis function. OTs are organometallic pollutants with a tin atom bound to one or more carbon atoms. OT exposure may occur through the food chain and/or contaminated water, since they have multiple applications in industry and agriculture. In addition, OTs have been used with few legal restrictions in the last decades, despite being highly toxic. In addition to their action as EDC, OTs can also cross the blood-brain barrier and show relevant neurotoxic effects, as observed in several animal model studies specifically involving the development of neurodegenerative processes, neuroinflammation, and oxidative stress. Thus, the aim of this short review is to summarize the toxic effects of the most common OT compounds, such as trimethyltin, tributyltin, triethyltin, and triphenyltin, on the brain with a focus on neuronal damage as a result of oxidative stress and neuroinflammation. We also aim to present evidence for the disruption of behavioral functions, neurotransmitters, and neuroendocrine pathways caused by OTs.

Keywords: behavioral impairments; brain function; endocrine disruptor; environmental contaminant; neurodegeneration; neuroinflammation; neurotoxicity; oxidative stress.

Figures

Figure 1
Figure 1
A possible pathway for tributyltin (TBT)-generated oxidative stress in neuronal cells. Considering the data of Ishihara and colleagues (41), supported by data of other groups, TBT leads to neuronal reactive oxygen species (ROS) production by a reduction in the estrogen levels, leading to impairments in the Akt signaling and subsequent downregulation of glutathione S-transferase (GST), an important antioxidant mechanism to protect neuronal normal function.

Similar articles

See all similar articles

Cited by 4 articles

References

    1. Colborn T, Vom Saal FS, Soto AM. Developmental effects of endocrine disrupting chemicals in wildlife and humans. Environ Health Perspect (1993) 101(5):378–84.10.1289/ehp.93101378 - DOI - PMC - PubMed
    1. Tabb M, Blumberg B. New modes of action for endocrine-disrupting chemicals. Mol Endocrinol (2006) 20(3):475–82.10.1210/me.2004-0513 - DOI - PubMed
    1. Elsworth JD, Jentsch JD, Groman SM, Roth RH, Redmond DE, Leranth C. Low circulating levels of bisphenol-A induce cognitive deficits and loss of asymmetric spine synapses in dorsolateral prefrontal cortex and hippocampus of adult male monkeys. J Comp Neurol (2015) 523(8):1248–57.10.1002/cne.23735 - DOI - PMC - PubMed
    1. Chopra V, Harley K, Lahiff M, Eskenazi B. Association between phthalates and attention deficit disorder and learning disability in U.S. children, 6–15 years. Environ Res (2014) 128:64–9.10.1016/j.envres.2013.10.004 - DOI - PMC - PubMed
    1. Leon-Olea M, Martyniuk CJ, Orlando EF, Ottinger MA, Rosenfeld C, Wolstenholme J, et al. Current concepts in neuroendocrine disruption. Gen Comp Endocrinol (2014) 203:158–73.10.1016/j.ygcen.2014.02.005 - DOI - PMC - PubMed

LinkOut - more resources

Feedback