Ben-Shahar Yehuda
Department of Biology, Washington University in St. Louis, St. Louis, MO, United States.
Front Genet. 2018 Mar 1;9:70. doi: 10.3389/fgene.2018.00070. eCollection 2018.
Manganese (Mn) is an essential trace element that acts as a metal co-factor in diverse biochemical and cellular functions. However, chronic environmental exposure to high levels of Mn is a well-established risk factor for the etiology of severe, atypical parkinsonian syndrome (manganism) via its accumulation in the basal ganglia, pallidum, and striatum brain regions, which is often associated with abnormal dopamine, GABA, and glutamate neural signaling. Recent studies have indicated that chronic Mn exposure at levels that are below the risk for manganism can still cause behavioral, cognitive, and motor dysfunctions via poorly understood mechanisms at the molecular and cellular levels. Furthermore, in spite of significant advances in understanding Mn-induced behavioral and neuronal pathologies, available data are primarily for human and rodents. In contrast, the possible impact of environmental Mn exposure on brain functions and behavior of other animal species, especially insects and other invertebrates, remains mostly unknown both in the laboratory and natural habitats. Yet, the effects of environmental exposure to metals such as Mn on insect development, physiology, and behavior could also have major indirect impacts on human health via the long-term disruptions of food webs, as well as direct impact on the economy because of the important role insects play in crop pollination. Indeed, laboratory and field studies indicate that chronic exposures to metals such as Mn, even at levels that are below what is currently considered toxic, affect the dopaminergic signaling pathway in the insect brain, and have a major impact on the behavior of insects, including foraging activity of important pollinators such as the honey bee. Together, these studies highlight the need for a better understanding of the neuronal, molecular, and genetic processes that underlie the toxicity of Mn and other metal pollutants in diverse animal species, including insects.
锰(Mn)是一种必需的微量元素,在多种生化和细胞功能中作为金属辅助因子发挥作用。然而,长期环境暴露于高水平的锰是严重非典型帕金森综合征(锰中毒)病因的一个公认风险因素,因为锰会在基底神经节、苍白球和纹状体脑区蓄积,这通常与多巴胺、γ-氨基丁酸(GABA)和谷氨酸神经信号异常有关。最近的研究表明,低于锰中毒风险水平的慢性锰暴露仍可通过分子和细胞水平上尚不清楚的机制导致行为、认知和运动功能障碍。此外,尽管在理解锰诱导的行为和神经元病理学方面取得了重大进展,但现有数据主要来自人类和啮齿动物。相比之下,环境锰暴露对其他动物物种,尤其是昆虫和其他无脊椎动物的脑功能和行为可能产生的影响,在实验室和自然栖息地大多仍不为人知。然而,环境暴露于锰等金属对昆虫发育、生理和行为的影响,也可能通过长期破坏食物网对人类健康产生重大间接影响,以及由于昆虫在作物授粉中发挥的重要作用而对经济产生直接影响。事实上,实验室和实地研究表明,长期暴露于锰等金属,即使是低于目前认为有毒的水平,也会影响昆虫大脑中的多巴胺能信号通路,并对昆虫行为产生重大影响,包括对重要传粉者如蜜蜂的觅食活动。总之,这些研究强调需要更好地理解锰和其他金属污染物在包括昆虫在内的多种动物物种中产生毒性的神经元、分子和遗传过程。