Chronic exposure to environmental cadmium affects growth and survival, cellular stress, and glucose metabolism in juvenile channel catfish (Ictalurus punctatus).
Chronic exposure to environmental cadmium affects growth and survival, cellular stress, and glucose metabolism in juvenile channel catfish (Ictalurus punctatus).
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DOI：
10.1016/j.aquatox.2020.105705
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发表时间：
2021-01
期刊：
影响因子：
--
通讯作者：
Small BC
中科院分区：
文献类型：
--
作者：
Paul JS;Small BC
人为活动导致淡水系统中镉的富集，镉是渔业和水产养殖业关注的污染物，因为它没有已知的生物功能，并且在痕量浓度下有毒。然而，关于长期暴露于环境相关浓度对淡水鱼的影响仍然存在知识差距。因此，本研究的目的是评估镉对斑点叉尾鮰（Ictalurus punctatus）的长期影响，包括随着时间的推移，组织特异性生物累积模式与这些组织的功能之间的关系。我们重点关注肝脏和肾脏，以及与细胞应激、葡萄糖代谢和类固醇生成相关的基因的表达。从受精到六个月，鲶鱼暴露于浓度为 0.5（对照）、2（低）和 6（高）μg L−1 Cd 的环境中。镉暴露会对斑点叉尾鮰的生长产生负面影响，并与组织镉的生物积累有关，这种积累遵循剂量相关的反应，其中躯干肾>肝脏=头肾>>肌肉中的浓度。处理之间还观察到组织中钙、铜、铁和锌浓度的差异。暴露 3 个月后，金属硫蛋白 (MT) 和热休克蛋白 (HSP) 70 和 90 的表达相对于对照有所增加；然而，在 6 个月时没有检测到差异，表明存在补偿。相反，类固醇生成、类固醇生成因子 1 (SF1)、类固醇生成急性调节蛋白 (StAR) 和细胞色素 P450scc (P450) 等关键基因的表达模式没有差异，这支持了镉不影响继发性应激反应的观察结果，通过低水分胁迫事件后的血浆皮质醇和葡萄糖浓度进行评估。作为长度和重量的函数，高镉处理产生的鱼明显小于对照。除了注意到 MT 和 HSP 中的细胞反应外，高镉处理中生长的减少可能至少部分是由于能量需求的增加。葡萄糖代谢所需基因上调的观察结果支持了这一点。暴露 3 个月后，与对照组相比，高剂量组的己糖激酶 (HK)、葡萄糖 6 磷酸酶 (G6P) 和甘油醛 3 磷酸脱氢酶 (GAPDH) 显着升高。在研究期间，暴露还使斑点叉尾鮰的存活时间减少了 3 至 6 个月。镉暴露导致的健康状况下降可能会通过生活史和生长模式的改变在人口层面上显现出来。
Anthropogenic activities have led to the enrichment of cadmium in freshwater systems where it is a contaminant of concern for fisheries and aquaculture as it has no known biological function and is toxic at trace concentrations. Yet, knowledge gaps remain regarding effects of chronic exposure to environmentally relevant concentrations on freshwater fish. Thus, the objectives of the current study were to assess chronic impacts of cadmium on channel catfish (Ictalurus punctatus) including how tissue-specific bioaccumulation patterns relate to functions of those tissues over time. We focused on liver and kidneys, and expression of genes related to cellular stress, glucose metabolism, and steroidogenesis. Catfish were exposed to concentrations of 0.5 (control), 2 (low), and 6 (high) μg L−1 Cd from fertilization to six months. Cadmium exposure negatively impacted channel catfish growth and was linked to bioaccumulation of tissue Cd, which followed a dose-related response, where concentrations in trunk kidney > liver = head kidney >> muscle. Differences in tissue Ca, Cu, Fe, and Zn concentrations were also observed between treatments. Following 3 months of exposure, expression of metallothionein (MT) and heat shock proteins (HSP) 70 & 90 increased relative to controls; however, no differences were detected at 6 months, suggesting compensation. Conversely, there were no differences in expression patterns for key genes in steroidogenesis, steroidogenic factor 1 (SF1), steroidogenic acute regulatory protein (StAR), and cytochrome P450scc (P450), which supports the observation that Cd did not affect the secondary stress response, evaluated via plasma cortisol and glucose concentrations following a low water stress event. As a function of length and weight, the high Cd treatment yielded fish that were significantly smaller than controls. In addition to the cellular responses in MT and HSPs noted, reduced growth in the high Cd treatment was likely due, at least in part, to elevated energetic demands. This is supported by observations of the upregulation of genes necessary for glucose metabolism. Hexokinase (HK), glucose-6-phosphatase (G6P), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were significantly elevated in the high treatment relative to controls at 3 months of exposure. Over the study period, exposure also reduced survival of channel catfish from 3 to 6 months. Reduced fitness, as a consequence of cadmium exposure, could be visible at the population level through altered life histories and growth patterns.
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影响因子：
4.1
作者：
Borgmann, U;Couillard, Y;Dixon, DG
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影响因子：
3.3
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影响因子：
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作者：
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影响因子：
5.2
作者：
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通讯作者：
Small BC