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.

人为活动导致镉在淡水系统中富集，在淡水系统中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，关于长期接触环境相关浓度对淡水鱼的影响，知识差距仍然存在。因此，当前研究的目的是评估镉对鲶鱼（Ictalurus punctatus）的慢性影响，包括组织特异性生物积累模式如何与这些组织的功能随着时间的推移而相关。我们专注于肝脏和肾脏，以及与细胞应激、葡萄糖代谢和类固醇生成相关的基因表达。鲶鱼暴露于 0.5（对照）、2（低）和 6（高）μg L ^{-1 的}浓度镉从受精到六个月。镉暴露对鲶鱼的生长产生负面影响，并与组织 Cd 的生物积累有关，后者遵循剂量相关反应，其中躯干肾 > 肝 = 头肾 > 肌肉中的浓度。在处理之间也观察到组织 Ca、Cu、Fe 和 Zn 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 的表达相对于对照增加；然而，在 6 个月时未检测到差异，表明有补偿。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) 中关键基因的表达模式没有差异，这支持了 Cd 不影响继发性应激反应的观察结果，通过低水分应激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。除了注意到的 MT 和 HSP 中的细胞反应外，高 Cd 处理的生长减少可能至少部分是由于能量需求增加。这得到了对葡萄糖代谢所需基因上调的观察结果的支持。在暴露 3 个月时，与对照组相比，在高剂量治疗中己糖激酶 (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，暴露也将沟鲶的存活时间从 3 个月缩短到 6 个月。