From Compensation to Collapse: UVB-Driven Disruption of Host–Microbiota Homeostasis Exacerbates Amphibian Ecological Risk

The synergistic effects of stratospheric ozone depletion and climate change are intensifying surface ultraviolet-B (UVB) radiation, posing a severe threat to amphibians-one of the most endangered vertebrate groups globally. <i>Xenopus laevis</i>, with its cutaneous respiration and limited photoprotective mechanisms, exhibits high sensitivity to UVB, making it a suitable model for ecotoxicological studies. While UVB is known to cause DNA damage, immune suppression, and microbial dysbiosis, its mechanisms in multi-organ interactions, dose-response thresholds, and host-microbiome regulatory networks remain poorly understood. This study employed a gradient UVB exposure regime integrated with histopathology, oxidative stress assays, and 16S rRNA sequencing to systematically evaluate the effects of UVB on (1) cascade damage across skin, liver, and intestinal barriers; (2) immune cell distribution; (3) redox dynamics; and (4) microbial community structure and function. Our findings demonstrate that low-dose UVB activated compensatory antioxidant defenses without structural disruption, whereas exposure beyond a critical threshold induced nonlinear redox collapse, microbial dysbiosis, and multi-organ barrier failure, collectively exacerbating ecological adaptation risks. These results reveal a cross-scale mechanism by which UVB impairs amphibian health via disruption of host-microbe homeostasis, providing a conceptual and empirical framework for assessing species vulnerability under ongoing climate change.