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生理生化响应和转录组分析揭示了磺胺甲恶唑对蛋白核小球藻固碳功能的影响及其作用机制。

Physiological-biochemical responses and transcriptomic analysis reveal the effects and mechanisms of sulfamethoxazole on the carbon fixation function of Chlorella pyrenoidosa.

机构信息

Co-Innovation center for sustainable Forestry in Southern China, College of Ecology and Environment, Nanjing Forestry University, Longpan Road 159, Nanjing 210037, Jiangsu, China; School of Chemical Engineering and Materials, Changzhou Institute of Technology, No. 666 Liaohe Road, Changzhou, Jiangsu 213032, China.

Co-Innovation center for sustainable Forestry in Southern China, College of Ecology and Environment, Nanjing Forestry University, Longpan Road 159, Nanjing 210037, Jiangsu, China; National Positioning Observation Station of Hung-tse Lake Wetland Ecosystem in Jiangsu Province, Hongze, Jiangsu 223100, China.

出版信息

Sci Total Environ. 2024 Mar 20;917:170460. doi: 10.1016/j.scitotenv.2024.170460. Epub 2024 Jan 28.

Abstract

The occurrence of sulfamethoxazole (SMX) is characterized by low concentration and pseudo-persistence. However, the toxic effects and mechanisms of SMX, especially for low concentration and long-term exposure, are still not clear. This study investigated the effects and mechanisms of SMX on carbon fixation-related biological processes of Chlorella pyrenoidosa at population, physiological-biochemical, and transcriptional levels. Results showed that 1-1000 μg/L SMX significantly inhibited the dry weight and carbon fixation rate of C. pyrenoidosa during 21 d. The upregulation of superoxide dismutase (SOD) and catalase (CAT) activities, as well as the accumulation of malondialdehyde (MDA) demonstrated that SMX posed oxidative damage to C. pyrenoidosa. SMX inhibited the activity of carbonic anhydrase (CA), and consequently stimulated the activity of Rubisco. Principal component analysis (PCA) revealed that SMX concentration was positively correlated with Rubisco and CAT while exposure time was negatively correlated with CA. Transcriptional analysis showed that the synthesis of chlorophyll-a was stabilized by regulating the diversion of protoporphyrin IX and the chlorophyll cycle. Meanwhile, multiple CO compensation mechanisms, including photorespiratory, C-like CO compensation and purine metabolism pathways were triggered in response to the CO requirements of Rubisco. This study provides a scientific basis for the comprehensive assessment of the ecological risk of SMX.

摘要

磺胺甲恶唑(SMX)的出现具有浓度低和假持久性的特点。然而,SMX 的毒性作用和机制,特别是对于低浓度和长期暴露的情况,仍然不清楚。本研究从种群、生理生化和转录水平调查了 SMX 对蛋白核小球藻(Chlorella pyrenoidosa)与碳固定相关的生物过程的影响及其机制。结果表明,在 21 天内,1-1000μg/L 的 SMX 显著抑制了蛋白核小球藻的干重和碳固定率。超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性的上调以及丙二醛(MDA)的积累表明 SMX 对蛋白核小球藻造成了氧化损伤。SMX 抑制碳酸酐酶(CA)的活性,从而刺激 Rubisco 的活性。主成分分析(PCA)表明,SMX 浓度与 Rubisco 和 CAT 呈正相关,而暴露时间与 CA 呈负相关。转录分析表明,通过调节原卟啉 IX 的分流和叶绿素循环,稳定了叶绿素-a 的合成。同时,为了满足 Rubisco 对 CO 的需求,触发了多种 CO 补偿机制,包括光呼吸、C 型 CO 补偿和嘌呤代谢途径。本研究为全面评估 SMX 的生态风险提供了科学依据。

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