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Amostras de solo provenientes de áreas que receberam a aplicação de imazaquin e trifluralin foram utilizadas na condução de bioensaios com milho em casa-de-vegetação. A toxicidade visual no milho cultivado em solo no qual foi aplicado trifluralin decresceu mais rapidamente do que no solo que recebeu a aplicação de imazaquin. Os resíduos de imazaquin provocaram redução no acúmulo de biomassa da parte aérea do milho, praticamente em todas as doses, até 60 dias após a aplicação (DAA), mas esse efeito só foi observável até 90 DAA, para doses acima de 180g/ha. Para as raízes, no entanto, o efeito foi mais prolongado e, somente a partir de 120 DAA, a redução no peso deixou de ser observada. O efeito dos resíduos de trifluralin sobre as plantas de milho manifestou-se de forma mais evidente sobre as raízes do que sobre a parte aérea, e a redução no crescimento radicular perceptível até os 150 DAA. Com relação às amostras coletadas na profundidade 10-20cm, observaram-se sintomas de toxicidade para imazaquin, sugerindo maior potencial de movimentação no perfil do solo.

The incidence of type 2 diabetes mellitus (T2DM) has increased in our society in recent decades as the population ages, and this trend is not expected to revert. This is the same for the incidence of the main neurodegenerative disorders, including the two most common ones, which are, Alzheimer’s and Parkinson’s disease. Currently, no pharmacological therapies have been developed to revert or cure any of these pathologies. Interestingly, in recent years, an increased number of studies have shown a high co-morbidity between T2DM and neurodegeneration, as well as some common molecular pathways that are affected in both types of diseases. For example, while the etiopathology of T2DM and neurodegenerative disorders is highly complex, mitochondrial dysfunction has been broadly described in the early steps of both diseases; accordingly, this dysfunction has emerged as a plausible molecular link between them. In fact, the prominent role played by mitochondria in the mammalian metabolism of glucose places the physiology of the organelle in a central position to regulate many cellular processes that are affected in both T2DM and neurodegenerative disorders. In this collaborative review, we critically describe the relationship between T2DM and neurodegeneration; making a special emphasis on the mitochondrial mechanisms that could link these diseases. A better understanding of the role of mitochondria on the etiopathology of T2DM and neurodegeneration could pave the way for the development of new pharmacological therapies focused on the regulation of the physiology of the organelle. These therapies could, ultimately, contribute to increase healthspan.