科研之友
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摘要
Zinc ion (Zn) is an essential nutrition element and it is important to understand its regulation and distribution among different cellular organelles. Here, subcellular trafficking of Zn in rabbitfish fin cells was investigated through bioim-aging, and the results showed that the toxicity and bioaccumulation of Zn were both dose-and time-dependent. Cyto-toxicity of Zn only occurred when the Zn concentration reached 200-250 mu M after 3 h of exposure when the cellular quota of Zn:P reached a threshold level around 0.7. Remarkably, the cells were able to maintain homeostasis at a low Zn exposure concentration or within the first 4-h exposure. Zn homeostasis was mainly regulated by the lysosomes which stored Zn within the short exposure period, during which the number and size of lysosomes as well as the lyso-zyme activity increased in response to incoming Zn. However, with increasing Zn concentration beyond a threshold concentration (> 200 mu M) and an exposure time > 3 h, homeostasis was disrupted, leading to an Zn spillover to cyto-plasm and other cellular organelles. At the same time, cell viability decreased due to the Zn damage on mitochondria which caused morphological changes (smaller and rounder dots) and over production of reactive oxygen species, in-dicating the dysfunction of mitochondria. By further purifying the cellular organelles, cell viability was found to be consistent with the mitochondrial Zn amount. This study suggested that the amount of mitochondrial Zn was an excel-lent predictor of Zn toxicity on fish cells.
