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高海拔和低海拔两栖动物对急性UVB暴露的差异生态毒理学响应机制研究

Differential ecotoxicological responses of high- and low-altitude amphibians to acute UVB exposure: an integrated analysis of skin, oxidative, and DNA repair mechanisms

Xiaolong Tang, Lun Jia, Liye Zhong, Zhaoxuan Zhai, Xueying Zhang, Tao Zhang, Zhiyi Niu, Peiyi Zhang, Huihui Wang, Miaojun Ma, Qiang Chen

Journal:JOURNAL OF HAZARDOUS MATERIALS

IF:11.3

DOI:10.1016/j.jhazmat.2026.141218

PMID:41604937

Published:2026-01-24

research field:神经科学蛋白质组学分子生物学细胞生物学阿尔茨海默病研究

Abstract

Acute increases in ultraviolet-B (UVB) radiation, driven by ozone depletion and climate change, function as a non-chemical environmental contaminant that can inflict rapid physiological and molecular damage. Yet ecotoxicological assessments focusing on acute high-intensity UV events are scarce. Here, we treat UVB as a hazardous environmental stressor and use the Qinghai–Tibetan Plateau endemic frog Rana kukunoris to compare high-altitude (HA) and low-altitude (LA) populations’ multi-level responses to a controlled acute UVB challenge (4   h, 1800 μW cm −2 ) and recovery (4–48   h post-exposure, HPE). By integrating skin histology/pigmentation, oxidative and antioxidant indices, DNA damage, apoptosis, and gene expression, we revealed pronounced altitude-dependent differences in defense strategies. HA frogs displayed a thicker epidermis and darker baseline pigmentation with a smaller UVB-induced darkening amplitude, whereas LA frogs had lighter baseline coloration and stronger darkening (reflectance minima at 4 HPE in both populations), together indicating contrasting pigmentary buffering capacities. HA frogs further showed rapid antioxidant mobilization (skin and liver T-AOC peaked at 4 HPE), faster DNA repair (alkaline comet tail length and TDNA% decreased at 5.3   AU   h −1 and 2.8% h −1 over 0–12 HPE), and apoptosis peaking at 12 HPE, indicating early containment with reduced downstream investment. LA frogs showed delayed antioxidant activation (T-AOC peaked at 24 HPE in skin and 12 HPE in liver), slower repair (3.6   AU   h −1 and 0.8% h −1 ), delayed apoptosis (24 HPE), and stronger hepatic induction of repair/apoptosis pathways (CPD photolyase 33.7-fold; OGG1 35.2-fold vs 2.8- and 6.4-fold in HA), consistent with compensatory, higher-demand responses. Together, these findings demonstrate that acute UVB exposure elicits altitude-specific, multi-level defense

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