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光酶促DNA修复在减轻幼虫UVB暴露的残留效应方面作用有限:对青蛙种群补充的影响

Limited contribution of photoenzymatic DNA repair in mitigating carry-over effects from larval UVB exposure: Implications for frog recruitment.

作者信息

Londero James Eduardo Lago, Viana Altevir Rossato, Silva Larissa Duailibe, Schavinski Cassiano Ricardo, Schuch André Passaglia

机构信息

Post-Graduation Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil; Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.

Post-Graduation Program in Biological Sciences: Toxicological Biochemistry, Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, RS, Brazil.

出版信息

Sci Total Environ. 2024 May 10;924:171647. doi: 10.1016/j.scitotenv.2024.171647. Epub 2024 Mar 11.

Abstract

Solar ultraviolet-B (UVB) radiation has increased due to stratospheric ozone depletion, climate and ecosystem changes and is a driver of amphibian population declines. Photoenzymatic repair (PER) is a critical mechanism for limiting UVB lethality in amphibian larvae. However, the link between PER and the UVB-induced effects remains understudied through long-term investigations in vivo. Here, we assessed how larval PER determines the lethal and sublethal effects induced by environmentally relevant acute UVB exposure until the juvenile phase in the Neotropical frog Odontophrynus americanus. We conducted laboratory-based controlled experiments in which tadpoles were or were not exposed to UVB and subsequently were exposed to light (for PER activation) or dark treatments. Results showed that the rates of mortality and apoptosis observed in post-UVB dark treatment are effectively limited in post-UVB light treatment, indicating PER (and not dark repair, i.e. nucleotide excision repair) is critical to limit the immediate genotoxic impact of UVB-induced pyrimidine dimers. Nonetheless, even tadpoles that survived UVB exposure using PER showed sublethal complications that extended to the juvenile phase. Tadpole responses included alterations in morphology, chromosomal instability, increased skin susceptibility to fungal proliferation, as well as increased generation of reactive oxygen species. The short-term effects were carried over to later stages of life because metamorphosis time increased and juveniles were smaller. No body abnormalities were visualized in tadpoles, metamorphs, and juveniles, suggesting that O. americanus is UVB-resistant concerning these responses. This study reveals that even frog species equipped with an effective PER are not immune to carry-over effects from early UVB exposure, which are of great ecological relevance as late metamorphosis and smaller juveniles may impact individual performance and adult recruitment to breeding. Future ecological risk assessments and conservation and management efforts for amphibian species should exercise caution when linking PER effectiveness to UVB resistance.

摘要

由于平流层臭氧消耗、气候和生态系统变化,太阳紫外线B(UVB)辐射增加,这是两栖动物种群数量下降的一个驱动因素。光酶修复(PER)是限制两栖动物幼体UVB致死率的关键机制。然而,通过长期的体内研究,PER与UVB诱导效应之间的联系仍未得到充分研究。在这里,我们评估了新热带蛙美洲齿蟾幼体的PER如何决定环境相关急性UVB暴露直至幼年期所诱导的致死和亚致死效应。我们进行了基于实验室的对照实验,其中蝌蚪暴露或未暴露于UVB,随后暴露于光照(用于激活PER)或黑暗处理。结果表明,在UVB后黑暗处理中观察到的死亡率和凋亡率在UVB后光照处理中得到有效限制,表明PER(而非黑暗修复,即核苷酸切除修复)对于限制UVB诱导的嘧啶二聚体的直接遗传毒性影响至关重要。尽管如此,即使使用PER在UVB暴露中存活下来的蝌蚪也表现出亚致死并发症,这些并发症一直持续到幼年期。蝌蚪的反应包括形态改变、染色体不稳定、皮肤对真菌增殖的易感性增加以及活性氧的产生增加。这些短期效应延续到了生命的后期阶段,因为变态时间增加且幼体较小。在蝌蚪、变态幼体和幼蛙中未观察到身体异常,这表明美洲齿蟾在这些反应方面对UVB具有抗性。这项研究表明,即使配备有效PER的蛙类也无法免疫早期UVB暴露的遗留效应,由于变态延迟和幼体较小可能会影响个体表现和成年个体参与繁殖,这些遗留效应具有重大的生态相关性。在将PER有效性与UVB抗性联系起来时,未来对两栖动物物种的生态风险评估以及保护和管理工作应谨慎行事。

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