Gómez-Mendikute A, Cajaraville M P
Laboratory of Cell Biology and Histology, Department of Zoology and Animal Cell Dynamics, University of the Basque Country, PO BOX 644, E-48080 Bilbao, Basque Country, Spain.
Toxicol In Vitro. 2003 Oct-Dec;17(5-6):539-46. doi: 10.1016/s0887-2333(03)00093-6.
The immune defence of mussels is comprised of cell-mediated and humoral mechanisms, in which haemocytes or blood cells play a key role. Environmental pollutants such as metallic and organic xenobiotics exert immunotoxical effects on aquatic organisms. Some of these xenobiotics are known to give rise to highly reactive oxygen species (ROS), thereby leading to oxidative damage to tissue macromolecules including DNA, proteins and lipids. Previously we have detected enhancement of ROS production together with severe alterations in the actin cytoskeleton after exposure of mussel haemocytes to the carcinogenic polycyclic aromatic hydrocarbon benzo[a]pyrene (b[a]p). In a similar way, cadmium is also known to cause disruption of the actin cytoskeleton in mussel haemocytes, however it is not known whether this effect occurs by direct action or through ROS production. The aim of the present study was to decipher whether cytoskeletal alterations caused by Cd in mussel haemocytes are linked to increased ROS production. ROS-producing model compounds copper (Cu), paraquat and b[a]p were used in parallel experiments for comparative purposes. In all contaminant exposure experiments actin cytoskeleton appeared damaged. On the other hand, ROS production was increased in paraquat and b[a]p exposure experiments but decreased in haemocytes exposed to Cu while no significant effects were detected in Cd exposure experiments. In conclusion, it appears that deleterious effects of Cu and Cd on the integrity of the actin cytoskeleton of haemocytes are not directly linked to ROS production, at least at the exposure conditions used in the present study.
贻贝的免疫防御由细胞介导和体液机制组成,其中血细胞发挥关键作用。金属和有机异源生物等环境污染物对水生生物具有免疫毒性作用。已知其中一些异源生物会产生高活性氧(ROS),从而导致包括DNA、蛋白质和脂质在内的组织大分子发生氧化损伤。此前我们检测到,贻贝血细胞暴露于致癌多环芳烃苯并[a]芘(b[a]p)后,ROS生成增加,同时肌动蛋白细胞骨架发生严重改变。同样,镉也会导致贻贝血细胞中的肌动蛋白细胞骨架破坏,但尚不清楚这种效应是通过直接作用还是通过ROS生成发生的。本研究的目的是弄清楚镉在贻贝血细胞中引起的细胞骨架改变是否与ROS生成增加有关。为了进行比较,在平行实验中使用了产ROS的模型化合物铜(Cu)、百草枯和b[a]p。在所有污染物暴露实验中,肌动蛋白细胞骨架似乎都受到了损伤。另一方面,在百草枯和b[a]p暴露实验中ROS生成增加,而在暴露于铜的血细胞中ROS生成减少,在镉暴露实验中未检测到显著影响。总之,至少在本研究使用的暴露条件下,铜和镉对血细胞肌动蛋白细胞骨架完整性的有害影响似乎与ROS生成没有直接关系。