Singh Rashmi, Hussain Md Arafat, Kumar Jai, Kumar Manmohan, Kumari Usha, Mazumder Shibnath
Immunobiology Laboratory, Department of Zoology, University of Delhi, Delhi 110 007, India.
Immunobiology Laboratory, Department of Zoology, University of Delhi, Delhi 110 007, India.
Aquat Toxicol. 2017 Nov;192:30-39. doi: 10.1016/j.aquatox.2017.09.006. Epub 2017 Sep 6.
The current study was aimed to understand the effects of chronic fluoride exposure on fish immune system. African sharp tooth catfish (Clarias gariepinus) were exposed to 73.45mg/L of fluoride corresponding to 1/10 96h LC for 30 d and the effects on general fish health and several immune parameters were studied. Chronic fluoride exposure led to significant alteration in serum biochemical parameters including alkaline phosphatase, alanine transaminase, aspartate transaminase, triglycerides, cholesterol and blood urea nitrogen levels revealing the detrimental effect of fluoride on general fish health. Upregulation in cytochrome P450 1A expression, both at mRNA and protein level suggested that fluoride activates the detoxification machinery in headkidney (HK) of C. gariepinus. Histopathological analysis of HK from exposed fish further revealed fluoride-induced hypertrophy, increase in melano-macrophage centers (MMCs) and the development of cell-depleted regions. Fluoride reduced headkidney somatic index (HKSI) and the phagocytic potential of headkidney macrophages (HKM). It induced caspase-3-dependent headkidney leukocyte (HKL) apoptosis, elevated superoxide generation and production of pro-inflammatory cytokine TNF-α besides suppressed T-cell proliferation in the exposed fish. We surmise the elevation in superoxide levels coupled with increased TNF-α production to be plausible causes of fluoride-induced HKL apoptosis. It is concluded that chronic fluoride exposure induces structure-function alterations in HK, the primary lymphoid organ in fish leading to impairment in immune responses.
本研究旨在了解长期氟暴露对鱼类免疫系统的影响。将非洲尖齿鲶(Clarias gariepinus)暴露于73.45mg/L的氟中,相当于1/10的96小时半数致死浓度,持续30天,并研究其对鱼类总体健康状况和若干免疫参数的影响。长期氟暴露导致血清生化参数发生显著变化,包括碱性磷酸酶、丙氨酸转氨酶、天冬氨酸转氨酶、甘油三酯、胆固醇和血尿素氮水平,揭示了氟对鱼类总体健康的有害影响。细胞色素P450 1A在mRNA和蛋白质水平的表达上调表明,氟激活了非洲尖齿鲶头肾(HK)中的解毒机制。对暴露鱼类的头肾进行组织病理学分析进一步显示,氟诱导了肥大、黑素巨噬细胞中心(MMCs)增加以及细胞缺失区域的形成。氟降低了头肾体细胞指数(HKSI)和头肾巨噬细胞(HKM)的吞噬潜力。它诱导了依赖半胱天冬酶-3的头肾白细胞(HKL)凋亡,提高了超氧化物的生成和促炎细胞因子TNF-α的产生,此外还抑制了暴露鱼类中的T细胞增殖。我们推测超氧化物水平的升高以及TNF-α产生的增加可能是氟诱导HKL凋亡的原因。得出的结论是,长期氟暴露会诱导鱼类主要淋巴器官头肾的结构功能改变,导致免疫反应受损。