Organotin compounds (OTs) are synthetic persistent organometallic xenobiotics widely used in several commercial applications. They exert well-described harmful effects in brain, liver, adipose tissue, and reproductive organs, as they are endocrine-disrupting chemicals (EDCs), but the effects in the kidneys are less known. The kidneys are especially vulnerable to environmental contaminants because they are a metabolizing site of xenobiotics, therefore, pollutants can accumulate in renal tissue, leading to impaired renal function and to several renal abnormalities. Individuals chronically exposed to OTs present a threefold increase in the prevalence of kidney stones. These compounds can directly inhibit H⁺/K⁺-ATPase in renal intercalated cells, resulting in hypokalemia, renal tubular acidity, and increased urinary pH, which is a known risk factor for kidney stones formation. OTs effects are not only limited to induce nephrolithiasis, its nephrotoxicity is also due to increased reactive oxygen species (ROS). This increase leads to lipid peroxidation, abnormal cellular function, and cell death. Combined, the enzymatic and non-enzymatic antioxidant defense systems become deficient and there is a consequent uncontrolled generation of ROS that culminates in renal tissue damage. Still, few epidemiological and experimental studies have reported renal impact correlated to OTs exposure. This lack of investigation of the complete effect of OTs in renal function and structure led us to perform this review reporting the main researches about this subject.

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.