Acquired thermotolerance (heat priming) enables organisms to withstand lethal heat stress after prior sublethal exposure. While documented in bivalves through survival analyses, histological mechanisms in gills—their primary environmental interface—remain unclear. This study investigated heat priming effects on Crassostrea angulata gills using four experimental groups: control, sublethal, priming (sublethal + lethal), and lethal. Histopathology (HE staining and SEM) and apoptosis (TUNEL) were analyzed under varying thermal regimes. Lethal stress induced more than 20% gill shrinkage (vs. control) with elevated mucus cell counts, while SEM revealed exacerbated filament breakage and ciliary loss. Priming pretreatment significantly reduced filament contraction and mitigated structural damage. TUNEL-positive cell density peaked in the lethal group, showing an eightfold increase over priming at 48 h, whereas priming and sublethal groups exhibited comparable level. These findings indicate that heat priming synergistically alleviates both mechanical damage (gill shrinkage/filament disruption) and TUNEL-detected cell-death signals during subsequent lethal stress. The study establishes a tissue-level foundation for understanding acquired thermotolerance in oysters. • Gill filaments contracted into rods after lethal heat, while heat priming preserved their teardrop shape. • Lethal heat stimulation caused cilia shedding and damage on gill filament in oysters. • Heat priming reduces heat-induced apoptosis in oyster gill cells, keeping rates low.
Chen et al. (Sun,) studied this question.
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