Phosphorus-potassium fertilizer exposure induces oxidative stress and riboflavin metabolism disruption in juvenile turbot (Scophthalmus maximus)

IF 4.4 3区 环境科学与生态学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Ying Tao , Xin Li , Lele Wu , Ting Qi , Xinlu Yue , Xian Li
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Abstract

Intensive agriculture's excessive fertilizer use significantly contributes to coastal nutrient pollution. While phosphorus's ecological impacts are recognized, the toxicity of combined phosphorus nutrients on marine life remains unclear. This study examined phosphorus-potassium fertilizer's (P-K fertilizer) effects on juvenile turbot (Scophthalmus maximus) via a 96-hour acute exposure experiment. Exposure solutions were prepared at environmentally relevant concentrations, resulting in elevated seawater phosphorus and potassium levels by 117.25 mg/L and 152.94 mg/L, respectively. Compound fertilizer aggravated multi-tissue damage, such as gill epithelial cell proliferation. Untargeted metabolomics identified that P-K fertilizer disrupts riboflavin metabolism, leading to reduced riboflavin levels. This deficiency impaired the production of flavin mononucleotide and flavin adenine dinucleotide. Meanwhile, excess potassium ions triggered Na+/K+ ATPase pump and gene of the renal outer medullary K+ channel to maintain ionic balance. Following riboflavin metabolism disruption, juvenile turbot exhibited impaired antioxidant capacity, with significantly decreased activities of glutathione peroxidase (by 54.5 %) and superoxide dismutase (by 12.6 %), a significant increase in catalase activity, obvious accumulation of malondialdehyde, and a reduction in total antioxidant capacity. The changes in related gene expression measured by real-time qPCR were consistent with the observed alterations in enzyme activities. Overall, compared to exposure to PO43−-P alone, the combined P-K fertilizer exposure resulted in more severe disruption of riboflavin metabolism and exacerbated oxidative damage in marine fish, indicating that K+ potentiated the adverse effects through synergistic interactions. This work provides critical insights for managing nutrient pollution in marine ecosystems and safeguarding coastal biodiversity and ecosystem services.

Abstract Image

磷钾肥暴露诱导大菱鲆幼鱼氧化应激和核黄素代谢紊乱。
集约化农业的过度施肥是造成沿海养分污染的重要原因。虽然磷的生态影响已被认识到,但磷营养物对海洋生物的毒性仍不清楚。通过96小时急性暴露试验,研究了磷钾肥对大菱鲆(Scophthalmus maximus)幼鱼的影响。在与环境相关的浓度下制备暴露溶液,导致海水中磷和钾含量分别升高117.25 mg/L和152.94 mg/L。复合肥加重了鳃上皮细胞增殖等多组织损伤。非靶向代谢组学发现,磷钾肥破坏核黄素代谢,导致核黄素水平降低。这种缺陷损害了黄素单核苷酸和黄素腺嘌呤二核苷酸的产生。同时,过量的钾离子触发Na+/K+ atp酶泵和肾外髓K+通道基因维持离子平衡。核黄素代谢紊乱后,大菱鲆幼鱼抗氧化能力受损,谷胱甘肽过氧化物酶和超氧化物歧化酶活性显著降低(降低54.5 %),超氧化物歧化酶活性显著降低(降低12.6 %),过氧化氢酶活性显著升高,丙二醛积累明显,总抗氧化能力降低。实时荧光定量pcr检测到的相关基因表达变化与观察到的酶活性变化一致。总体而言,与PO43- P单独暴露相比,磷钾肥复合暴露导致海洋鱼类核黄素代谢受到更严重的破坏,并加剧了氧化损伤,这表明K+通过协同作用增强了不利影响。这项工作为管理海洋生态系统中的营养污染和保护沿海生物多样性和生态系统服务提供了重要见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.50
自引率
5.10%
发文量
206
审稿时长
30 days
期刊介绍: Part C: Toxicology and Pharmacology. This journal is concerned with chemical and drug action at different levels of organization, biotransformation of xenobiotics, mechanisms of toxicity, including reactive oxygen species and carcinogenesis, endocrine disruptors, natural products chemistry, and signal transduction with a molecular approach to these fields.
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