Journal of thermal biology最新文献

Heat stress (HS) and deoxynivalenol (DON) are two major stressors that significantly harm animals in livestock production. This research aims to analyze the joint impact of DON and heat stress on the gut health of male mice and to delve into the mechanisms behind it. After establishing a graded heat stress model and determining an appropriate exposure temperature, 48 male ICR (Institute of Cancer Research) mice were randomly allocated to four groups: control group (C), heat stress group (42 °C for 2 h, H), DON exposure group (receiving 2.5 μg DON/kg/day, D), and combined heat stress and DON exposure group (DH). After 14 days of model establishment, duodenal microbiota profiles were analyzed by sequencing, and indicators of duodenal injury were assessed using histological, molecular biological, and immunological methods. The findings showed that simultaneous exposure to DON and heat stress greatly aggravated intestinal harm in mice, as indicated by the shortening of intestinal villi, deepening of crypts, and decreased tight junction protein expression, which results in increased intestinal permeability. Additionally, the combined stress significantly increased the expression of inflammatory factors in the intestine, suggesting that the exacerbated inflammatory response played a pivotal role in aggravating intestinal damage. Mechanistic studies indicated that DON and heat stress alter the gut microbiota, stimulate the NF-κB signaling pathway, and encourage the release of inflammatory factors, indirectly affecting the function of the intestinal barrier. According to our study, the combined effects of DON and heat stress lead to intensified intestinal damage in male mice by impairing the intestinal barrier function and initiating inflammatory response pathways. These discoveries enhance our understanding of how environmental factors affect intestinal health and provide a foundation for developing preventive and therapeutic measures for associated diseases.

Environmental temperature can critically impact the performance and survival of ectotherms. Assessing the ability to tolerate increasing temperatures and determining coping strategies, especially in vulnerable taxa such as amphibians, is therefore crucial. Yet, little is known about the thermal traits of amphibians in megadiverse regions such as Asia. Here, we studied the widespread Asian Common Toad, Duttaphrynus melanostictus, and examined the role of behaviour in coping with extreme heat in adults and tadpoles. When provided with a thermal gradient, tadpoles avoided temperatures close to their CT_max, spending ∼96% of their time in the cooler water at the bottom of the water column, whereas adults selected lower temperatures under dry conditions compared to wet conditions. We also determined thermal tolerance limits across three ontogenetic stages: tadpoles, juveniles, and adults. The thermal tolerance limits of this species ranged from 6 to 43 °C. Critical thermal maxima (CT_max) varied across life stages, with the highest values observed in tadpoles, followed by adults and juveniles. Critical thermal minima (CT_min) were lowest in adults, followed by juveniles and tadpoles. Juveniles had the narrowest thermal breadth compared to adults and tadpoles. Thermal tolerance limits were independent of sex and body size in adults. Our work provides a detailed understanding of the thermal envelope for the widespread yet understudied tropical amphibian, D. melanostictus. By also examining thermoregulatory behaviours, our work presents insight into how thermal traits shift across life stages, with implications for forecasting species responses to future warming.

Heat stress is a major environmental factor limiting goat productivity. This study investigated the regulatory effects of creatine pyruvate (CrPyr) and γ-aminobutyric acid (GABA) on the antioxidant capacity and ruminal epithelial barrier function of goats under heat stress. A total of 54 Jianzhou large black goats, 4 months old with an average weight of 22.61 ± 0.47 kg, were randomly assigned to three groups: a control group (basic diet), a CrPyr group (basic diet with 0.4% CrPyr), and a GABA group (basic diet with 0.016% rumen-protected GABA). All goats were housed in an environment with temperatures ranging from 32 °C to 38 °C for 60 days. Physiological, serum, and ruminal parameters were measured. Results indicated that after 60 days, both CrPyr and GABA supplementation significantly increased serum levels of immunoglobulins (IgM, IgG) and decreased malondialdehyde (MDA) (P < 0.05). The CrPyr group exhibited elevated triiodothyronine (T3) and thyroxine (T4), while the GABA group showed higher T4 and glutathione peroxidase (GSH-Px) activity (P < 0.05). Ruminal epithelial morphology was improved in both treatment groups, evidenced by increased granular layer thickness in the dorsal rumen and decreased stratum corneum thickness in the ventral rumen (P < 0.05). Additionally, mRNA expression of pro-inflammatory cytokines (IL-1β, TNF-α) was downregulated, whereas expression of the anti-inflammatory cytokine IL-10 and tight junction proteins (Claudin-1, Occludin, ZO-1) was upregulated in the ruminal epithelium (P < 0.05). Transcriptome and KEGG analyses revealed that differentially expressed genes (e.g., ENO2, TNFAIP3) were primarily enriched in pathways related to energy metabolism, immune regulation, and oxidative stress, contributing to enhanced ruminal barrier function and heat stress adaptation. In summary, dietary supplementation with CrPyr or GABA enhances systemic antioxidant and immune capacity, promotes the repair of heat stress-induced ruminal epithelial damage, optimizes barrier function, and consequently mitigates the adverse effects of heat stress in goats.

Thermal stress from global warming and heated discharges from coastal nuclear power plants poses a significant threat to marine aquaculture, particularly during the sensitive early life stages of fish. These discharges elevate local seawater temperatures, altering the nearshore thermal environment. This study examined the effects of elevated temperatures on early development in large yellow croaker (Larimichthys crocea), a commercially important mariculture species in China. Embryos were exposed to five temperature regimes (22, 23, 24, 26 and 28 °C) to evaluate impacts on hatching success, survival, morphology, physiology, antioxidant activity, and immune gene expression. Temperatures +4 °C and +6 °C above the optimal 22 °C significantly reduced survival and body length, induced early hatching, and increased deformities. Antioxidant enzyme activity declined, while malondialdehyde (MDA) levels rose, indicating oxidative stress. Expression of heat shock proteins showed a selective response, with hsp70 downregulated and hsp27 upregulated. Immune-related genes such as nfkb and casp1 were upregulated, while infy, myd88, and tgfb were suppressed. The integrated biomarker response version 2 (IBRv2) quantified cumulative biological stress across treatments. These findings provide insight into the temperature sensitivity of early developmental stages in marine fish and emphasize the importance of thermal assessments under changing environmental temperature conditions.

Climate-driven increases in mean water temperature and the frequency of heatwaves affect the thermal tolerance of ectotherms, including fishes. Fishes can increase their thermal tolerance through acclimation, optimizing survival during extreme weather events. Few studies have investigated the exposure duration necessary for individuals to acclimate to warmer conditions or differences in acclimation dynamics among populations, limiting our understanding of how species deal with acute heat stress. Warmer waters can also increase parasite transmission. Although infections can reduce host thermal tolerance, the impact of parasite prevalence and abundance on fish acclimation capacity has not been explored, and may help explain population-level differences in thermal tolerance. We assessed thermal tolerance and acclimation dynamics across three populations of pumpkinseed sunfish (Lepomis gibbosus) from lakes in Quebec, Canada, differing in trematode and cestode infection prevalence. Pumpkinseed were acclimated to 22 °C or 27 °C from 3 h to 60 days before measuring critical thermal maximum (CT_max). CT_max increased with acclimation duration, with detectable increases after only 3 h, indicating rapid induction of acclimatory mechanisms. Fish from all populations appeared to reach full acclimation after 10 days at 27 °C. However, thermal tolerance was consistently highest in the control lake (Lake Triton, no cestodes or trematodes) compared to populations with intermediate (Lake Croche) and high (Lake Cromwell) infection prevalence, despite no relationship with parasite abundance. Although our design does not permit causal inference, these results suggest pumpkinseed rapidly acclimate to higher temperatures, but natural exposure to parasites could contribute to population-level differences in thermal tolerance.

Heat stress (HS) triggers reactive oxygen species (ROS) accumulation and activates stress-responsive signaling pathways, including c-Jun N-terminal kinase (JNK) and nuclear factor kappa B (NF-κB) in fish hepatocytes. However, how ROS, JNK, and NF-κB interact under HS and recovery remains poorly understood. In this study, we investigated these interactions in largemouth bass primary hepatocytes. First, we examined intracellular ROS levels and activation of JNK and NF-κB in hepatocytes immediately after HS (37 °C, 2 h) and during recovery (2, 6, 12, and 24 h). ROS levels and phosphorylated JNK significantly increased after HS and remained elevated throughout recovery, while NF-κB activation was observed at 6, 12, and 24 h after HS. Next, their regulatory relationship was investigated by pretreating hepatocytes with specific inhibitors prior to HS and allowing a 24-h recovery. JNK inhibitor SP600125 had no effect on ROS accumulation, whereas the ROS inhibitor N-acetylcysteine significantly reduced JNK activation, suggesting that ROS is functionally associated with JNK activation in this context. Furthermore, inhibition of either JNK or ROS significantly suppressed NF-κB activation, whereas the NF-κB inhibitor BAY11-7082 led to increased ROS accumulation and JNK activation, indicating a possible compensatory mechanism. Finally, we assessed whether these three signaling molecules regulate HS-induced apoptosis in hepatocytes. Inhibiting ROS or JNK reduced apoptosis, increased mitochondrial membrane potential, and decreased Caspase-3 activity. In contrast, NF-κB inhibition enhanced apoptosis. Collectively, our findings indicate that NF-κB may plays a protective role during HS recovery in fish by attenuating apoptosis through modulation of ROS/JNK signaling.