Integration of transcriptome, histopathology, and physiological indicators reveals regulatory mechanisms of largemouth bass ( Micropterus salmoides) in response to carbonate alkalinity stress

文献类型： 外文期刊

第一作者： Hua, Jixiang

作者： Hua, Jixiang;Xi, Bingwen;Qiang, Jun;Hua, Jixiang;Tao, Yifan;Lu, Siqi;Li, Yan;Dong, Yalun;Jiang, Bingjie;Xi, Bingwen;Qiang, Jun

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关键词： Micropterus salmoides; Carbonate alkalinity stress; Tissue damage; Serum biological chemistry; RNA-seq

期刊名称：AQUACULTURE （ 影响因子：3.9； 五年影响因子：4.4 ）

ISSN： 0044-8486

年卷期： 2025 年 596 卷

页码：

收录情况： SCI

摘要： The use of saline-alkali water resources is an important initiative for freshwater aquaculture. Largemouth bass (Micropterus salmoides) shows some salinity tolerance, but little is known about its alkali adaptation mechanism. First, we determined the 96-h 50 % lethal dose of alkaline carbonate (96-h LC50) for largemouth bass (41.41 mmol/L). Then, largemouth bass were subjected to 96-h carbonate alkalinity treatments and their responses were determined on the basis of histopathological, biochemical, and transcriptome analyses. The experiment included a control group (CA0, 0.49 mmol/L) and two treatment groups (CA20, 20 mmol/L; CA45, 45 mmol/L). The gill and liver tissues of the CA45 group exhibited severe deformation, including a thickened matrix, gill cell detachment, hepatocyte swelling, increased vacuolization, and localized necrotic lesions. In the CA20 group, some gill filaments were curled and deformed, hepatocytes had migrated, and tissue damage was minor. Both groups showed a lower percentage of apoptotic cells in gill and liver tissues. Serum antioxidant capacity first increased and then decreased, whereas energy metabolism and hormone indexes significantly increased under alkaline carbonate stress. Liver injury in the CA45 group resulted in significantly lower levels of cortisol, lactate dehydrogenase, and total protein compared with those in the CA20 group (P < 0.05). Transcriptome analyses of gill tissues from the CA45 group revealed significant alterations in pathways related to steroid biosynthesis (sqlea, lss, msmo1, tm7sf2), terpenoid backbone biosynthesis (hmgcs1, fdps, hmgcra, mvda), and ECM-receptor interaction and focal adhesion (col1a, col2a1b, col9a, col6a) due to alkalinity stress. These results indicate that liver damage under high alkalinity stress inhibits energy supply, while gill cell dysregulation triggers gill lesions.

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