Exploring the Influence of Heat Stress on Gene Expression in Bovine Myeloid Cells InVitro.

Effect of nutritional immunomodulation and heat stress during the dry period on subsequent performance of cows.

Effects of heat stress on energetic metabolism in lactating Holstein cows

Even though high temperatures significantly reduce both vegetative growth and yield in cotton, very little is known about the effects of heat stress on cotton antioxidant system. Thus, the effects of gradual heat stress on cotton growth in controlled conditions were investigated in the present study. At squaring stage, cotton plants were subjected to two different temperatures, 38 and 45°C to determine the influence of heat stress on the plants. The results of the present study showed that heat stress did not significantly altered the levels of malondialdehyde (MDA) and hydrogen peroxide (H2O2) in the leaves, whereas there was a remarkable decline in proline quantity of the leaves of plants subjected to 45°C heat stress. As for the amount of total chlorophyll content, a slight increase at plants treated with 38°C temperature was observed. Furthermore, the activities of some enzymes such as superoxide dismutase (SOD), which were associated with heat stress response in other plants was also investigated. For example, there was decline in the activitity ofSOD in the plants exposed to high temperatures. On the contrary, catalase (CAT)activity increased at 45°C; peroxidase (POX) activity increased at 38°C and ascorbate peroxidase (APX) activity increased at 38 and 45°C. The results from this study suggest a potential role for CAT, POX and APX in the reduction of elevated levels of H2O2 in cotton plants grown under heat stress condition. To sum up, it could be concluded that, diurnal gradual heat stress caused a low oxidative injury in cotton. Key words: Antioxidant enzymes, cotton, heat stress, lipid peroxidation, proline.

Coker, NA, Wells, AJ, and Gepner, Y. The effect of heat stress on measures of running performance and heart rate responses during a competitive season in male soccer players. J Strength Cond Res 34(4): 1141-1149, 2020-Measures of running performance and heart rate (HR) responses to match play during 3 different heat stress (HS) conditions were assessed in 7 National Collegiate Athletic Association (NCAA) Division I male soccer players. Total distance and distance covered within distinct velocity zones (walking [WALK], jogging [JOG], low-speed running, high-speed running, sprinting [SPRINT], low-intensity running [LIR], and high-intensity running [HIR]) were assessed using global positioning system units for more than 12 matches. Heat stress was monitored during each match, and matches were defined as low (HSlow, n = 4), moderate (HSmod, n = 4), or high (HShigh, n = 4) HS. Minutes played were significantly different across HS conditions (p = 0.03). Therefore, distance covered within each movement velocity was assessed relative to minutes played and as a percentage of total playing time. WALKrel was significantly greater during HShigh compared with HSlow (p = 0.035). LIRrel was significantly greater during HSmod (p = 0.015) compared with HSlow. A trend was observed for %WALK being higher during HShigh compared with HSlow (p = 0.066). %LIR was significantly greater during HShigh compared with HSlow (p = 0.048). High-intensity running was not significantly different across HS conditions. Percent of time spent >85% HRmax was significantly greater during HShigh (p = 0.002) and HSmod (p < 0.001) compared to HSlow. Percent of time spent between 65-84% HRmax was significantly greater during HSlow compared to HShigh (p < 0.001). Results indicate that HS resulted in increased LIR and %HR≥85, while HIR was maintained. High-intensity running performance may be conserved through decreased playing time or the adoption of pacing strategies. This may assist coaches in altering player management strategies to optimize team performance.

With climate change, selection for water efficiency and heat resilience are vitally important. We undertook this study to determine the effect of chronic cyclic heat stress (HS) on the hypothalamic expression profile of water homeostasis‐associated markers in high (HWE)‐ and low (LWE)‐water efficient chicken lines. HS significantly elevated core body temperatures of both lines. However, the amplitude was higher by 0.5–1°C in HWE compared to their LWE counterparts. HWE line drank significantly less water than LWE during both thermoneutral (TN) and HS conditions, and HS increased water intake in both lines with pronounced magnitude in LWE birds. HWE had better feed conversion ratio (FCR), water conversion ratio (WCR), and water to feed intake ratio. At the molecular level, the overall hypothalamic expression of aquaporins (AQP8 and AQP12), arginine vasopressin (AVP) and its related receptor AVP2R, angiotensinogen (AGT), angiotensin II receptor type 1 (AT1), and calbindin 2 (CALB2) were significantly lower; however, CALB1 mRNA and AQP2 protein levels were higher in HWE compared to LWE line. Compared to TN conditions, HS exposure significantly increased mRNA abundances of AQPs (8, 12), AVPR1a, natriuretic peptide A (NPPA), angiotensin I‐converting enzyme (ACE), CALB1 and 2, and transient receptor potential cation channel subfamily V member 1 and 4 (TRPV1 and TRPV4) as well as the protein levels of AQP2, however it decreased that of AQP4 gene expression. A significant line by environment interaction was observed in several hypothalamic genes. Heat stress significantly upregulated AQP2 and SCT at mRNA levels and AQP1 and AQP3 at both mRNA and protein levels, but it downregulated that of AQP4 protein only in LWE birds. In HWE broilers, however, HS upregulated the hypothalamic expression of renin (REN) and AVPR1b genes and AQP5 proteins, but it downregulated that of AQP3 protein. The hypothalamic expression of AQP (5, 7, 10, and 11) genes was increased by HS in both chicken lines. In summary, this is the first report showing improvement of growth performances in HWE birds. The hypothalamic expression of several genes was affected in a line‐ and/or environment‐dependent manner, revealing potential molecular signatures for water efficiency and/or heat tolerance in chickens.

Heat stress negatively affects reproductive functions in cows. Increased temperature disturbs fetal development in utero. However, the effect of heat stress on uterine endometrial tissues has not been fully examined. Using qPCR analysis, we measured the mRNA expression of various molecular markers in uterine endometrial tissue of dairy cows from Hokkaido, Japan, in winter and summer. Markers examined were heat shock proteins (HSPs), antioxidant enzymes (catalase, copper/zinc superoxide dismutase, manganese superoxide dismutase, and glutathione peroxidase 4), inflammatory cytokines, and interferon stimulated genes. Our results showed heat stress, body and milk temperatures were higher during summer than during winter. Expression levels of HSP27, HSP60, and HSP90 mRNA, and of catalase and copper/zinc superoxide dismutase mRNA were lower in summer than in winter. Tumor necrosis factor alpha expression was higher in summer than in winter. In conclusion, summer heat stress may reduce the expression of HSPs, affecting the levels of inflammatory cytokines in bovine uterine endometrial tissue.

Postnatal heat stress negatively impacts pig productivity and well-being as animals attempt to manage the resultant strain response. This is especially true when postnatal heat stress is combined with production stressors (e.g., mixing, weaning, transport, handling, and isolation) that have the potential to increase disease occurrence, morbidity and mortality. While pigs can utilize adaptive physiological mechanisms to compensate, these are often unfavorable to efficient livestock production. Specifically, postnatal heat stress decreases weight gain, reduces growth and production efficiency, alters carcass composition, and increases morbidity and mortality. Consequently, decreased animal performance constrains profitability and affects economic sustainability. In addition to the negative effects of postnatal heat stress, prenatal heat stress has long-term consequences that may compromise future piglet well-being and performance. Pigs gestated under heat stress conditions have an increased postnatal stress response and an increase in maintenance energy requirements. Furthermore, prenatal heat stress decreases swine birth weight, and increases teratogenicity, core body temperature set-point, and alters postnatal body composition (more adipose tissue and less skeletal muscle). Taken together, the effects of heat stress during pre- and postnatal pig development negatively influences productivity and well-being, a scenario that threatens the sustainability of global swine production.

The main reason for the maize genotype "DKC7221" to be heat tolerant is to have higher photosynthetic activity under heat stress conditions. The genotype "P3167" is sensitive to high temperature because of the heat-induced inhibition in photosynthetic electron transport reactions. In the present study, the effect of heat stress (45ºC for 20min) on some physiological changes was investigated through a chlorophyll afluorescence technique, and some endogenous resistance mechanisms (activities of some antioxidant enzymes, free proline, and reduced ascorbate contents) in two maize cultivars (Zea mays L. cvs. P3167 and DKC7221). Chlorophyll fluorescence measurements demonstrated that heat stress led to the reduction in the efficiency of the Hill reaction, accumulation of inactive reaction centers, inhibition of electron flow from reaction centers to the plastoquinone pool, and induction of non-photochemical dissipation of absorbed light energy. Changes in Φo/(1 - Φo), SFIABS and PIABS indicated that electron transport reactions in P3167 were almost completely inhibited by heat stress. In DKC7221, however, photosynthetic electron transport reactions were maintained under heat stress conditions. As a result of impairment in the photosynthetic efficiency in P3167 under heat stress, oxidative stress appeared as shown by lower antioxidant activity, accumulation of H2O2, malondialdehyde, and formazon and photooxidative injuries in chlorophyll pigments in the leaf tissue. DKC7221, on the other hand, had a higher antioxidant efficiency and lower oxidative damage under heat stress. FeSOD activity was found to be responsible for the dismutation of superoxide radicals in both maize genotypes under heat stress. As a result, it may be concluded that the genotype DKC7221 is more tolerant to heat stress than P3167.

Effect of season and temperature before and after calving on the future milk production of born heifers

The effects of whole-body heat stress on sympathetic and cardiovascular responses to stimulation of muscle metaboreceptors and mechanoreceptors remain unclear. We examined the muscle sympathetic nerve activity (MSNA), renal blood velocity, blood pressure and heart rate in 14 young healthy subjects during fatiguing isometric handgrip exercise, post exercise circulatory occlusion (PECO), and passive muscle stretch during PECO. The protocol was performed under normothermic and whole-body heat stress (increase internal temperature ~0.6 °C via a heating suit) conditions. Heat stress increased the resting MSNA and heart rate. Heat stress did not alter the responses to the fatiguing exercise in mean blood pressure (MAP), heart rate and MSNA, but augmented the response in renal vascular resistance (Δ45± 6 to Δ60±8 %, P=0.04). During PECO, the increase in MAP was lower during heat stress condition than during normothemic condition (Δ20±2 vs. Δ12±1 mmHg, P<0.001), while the increases in MSNA were not different between the thermal conditions (Δ16.4±2.8 vs. Δ17.3±3.8 bursts/min, P=0.74). Under normothermic conditions, the passive stretch during PECO evoked significant increases in MAP and MSNA, while these intervention did not alter MSNA or MAP in the presence of heat stress. These data show that the pressor response to metaboreceptor stimulation is attenuated, and the MSNA response to mechanoreceptor stimulation is also attenuated in heat stress condition. These observations suggest that whole body heat stress alters exercise pressor reflex in humans.

This study examined the effects of heat stress (HS) (41°C) and amino acid treatments, including citrulline (CIT) and arginine (ARG), on muscle-related gene expression in bovine myocytes. We hypothesized that CIT would increase ARG availability, which increases protein synthesis and myotube formation under HS conditions. Bovine satellite cells were isolated from a female fetus (23.1 kg) and plated at a density of 4 × 10⁴ cells in DMEM containing 10% FBS. The cells were incubated at 38°C with 5% CO₂ until they reached 80% confluency. The culture medium was replaced with differentiation medium (control media) consisting of 2% HS SILAC DMEM Flex Media (DMEM without ARG and CIT). The treatment groups were as follows: T1 (control media), T2 (control media with 120 µM ARG), and T3 (control media with 120 µM CIT). The cells were exposed to 38°C or 41°C, and harvested at 48 hours after temperature exposure. Real-time q-PCR was used to determine the gene responses related to HS and muscle growth for all treatment groups. The cells were stained to determine the differentiation fusion index and muscle fiber size. Data was analyzed using two-way ANOVA to evaluate the effects of treatments, temperature, and their interaction on gene expression, differentiation fusion index, and muscle fiber size. Tukey’s test was used for post-hoc comparisons. Results are presented as significant at P &amp;lt; 0.05. Analyses were conducted using GraphPad Prism 9.4.1 to assess treatment effects under normal and HS conditions. Gene expression of IGF-I was affected by treatment (P = 0.013) and its interaction with temperature (P = 0.003), with the highest expression in the CIT group under HS. Myf5 decreased with heat and ARG treatment (P &amp;lt; 0.001, P = 0.006). MyoD increased at 41°C (P = 0.015), with the highest levels in control. Myogenin was upregulated under HS, especially with CIT (P &amp;lt; 0.001, P = 0.004). Expression of MHC I was elevated with ARG at 41°C (P &amp;lt; 0.001). MHC ⅡA was affected by the interaction (P = 0.018), while MHC ⅡX expression was influenced by treatment (P = 0.01) and temperature (P= 0.015). Heat stress altered gene expression, with CIT enhancing IGF-1 and myogenin, while ARG increased MHC I. At 38°C, the treatments were statistically different (P=0.004) from one another with CIT (34.0%) being the highest. There were no differences between treatments in myotube length (P=0.820) or width (P=0.34) at 38°C. At 41°C, CIT and ARG treatments were both significantly different (P&amp;lt; 0.001) than control and both caused a greater myotube length (P=0.007). However, there was no difference in myotube width (P = 0.760). Therefore, CIT and ARG can increase fusion index and myotube length during times of HS while not affecting myotube width.

This study examined the effects of heat stress on the physiological functions and reproductive performance of dairy cows, emphasising the influence of cooling techniques, dietary interventions, and exposure to heat stress. This study employed a randomised controlled trial (RCT) methodology, involving two groups of dairy cows subjected to either heat stress conditions (30–35°C and 70–85% humidity) or thermoneutral settings (18–22°C and 45–55% humidity) conducted at UVAS, Lahore. Both groups received conventional or high-energy foods together with cooling measures (fans, misters, and shade). Physiological indicators, such as cortisol levels, body temperature, and respiration rates, were assessed in conjunction with oestrus cycles, ovulation rates, and pregnancy outcomes. The results indicated that heat stress markedly diminished milk production and reproductive health, characterised by prolonged estrous cycles, decreased ovulation rates, and lower pregnancy rates in the heat stress cohort. Cooling systems and nutritional techniques alleviated certain adverse effects; however, heat stress resulted in inferior outcomes relative to the control group. These results provide significant insights into how integrated management techniques can enhance dairy output and fertility rates under heat-stressed conditions. The research yielded substantial implications for dairy production operations, particularly in tropical and subtropical locations, where heat stress is a considerable issue. Future studies should focus on longitudinal studies regarding the effects of heat stress and genetic adaptation in dairy cattle, in addition to exploring the practical uses of cooling and nutritional therapies.

Simple SummaryHeat stress exerts extensive and intricate effects on germ cells, attracting significant attention from researchers. This article provides a comprehensive review and summary of the impacts and mechanisms of heat stress on ovarian granulosa cells. The systematic evaluation of heat stress effects on ovarian granulosa cells encompasses alterations in steroid hormone levels, oxidative stress, apoptosis, and mitochondrial function, with detailed discussions on several key mechanisms. Furthermore, this study analyzes the mechanism and potential relevance of ferroptosis in ovarian granulosa cells under heat stress conditions. Looking ahead to the future, gaining a deeper understanding of this complex mechanism will serve as a theoretical foundation for exploring possible interactions between heat stress and ferroptosis.Heat stress has been one of the key research areas for researchers due to the wide-ranging effects and complex mechanisms of action of its stress product reactive oxygen species (ROS). The aim of this paper is to comprehensively review and summarize the effects of heat stress on ovarian granulosa cells and their mechanism of action. We systematically reviewed the effects of heat stress on ovarian granulosa cells, including intracellular steroid hormone changes, oxidative stress, apoptosis, and mitochondrial function. Meanwhile, this paper discusses in detail several major mechanisms by which heat stress induces apoptosis in ovarian granulosa cells, such as through the activation of apoptosis-related genes, induction of endoplasmic reticulum stress, and the mitochondrial pathway. In addition, we analyzed the mechanism of ferroptosis in ovarian granulosa cells under heat stress conditions, summarized the potential association between heat stress and ferroptosis in light of the existing literature, and explored the key factors in the mechanism of action of heat stress, such as the signaling pathways of Nrf2/Keap1, HSPs, and JNK, and analyzed their possible roles in the process of ferroptosis. Finally, this paper provides an outlook on the future research direction, describing the possible interaction between heat stress and ferroptosis, with a view to providing a theoretical basis for further understanding and revealing the complex mechanism of ferroptosis occurrence in ovarian granulosa cells under heat stress.

Fetal programming in dairy cows: Effect of heat stress on progeny fertility and associations with the hypothalamic-pituitary-adrenal axis functions

BackgroundHeat stress in laying hens negatively affects egg production and shell quality by disrupting the homeostasis of plasma calcium and phosphorus levels. Although the kidney plays an important role in calcium and phosphorus homeostasis, evidence regarding the effect of heat stress on renal injury in laying hens is yet to be elucidated. Therefore, the aim of this study was to evaluate the effects of chronic heat stress on renal damage in hens during laying periods.MethodsA total of 16 white-leghorn laying hens (32 weeks old) were randomly assigned to two groups (n = 8). One group was exposed to chronic heat stress (33 °C for 4 weeks), whereas the other group was maintained at 24 °C.ResultsChronic heat exposure significantly increased plasma creatinine and decreased plasma albumin levels (P < 0.05). Heat exposure also increased renal fibrosis and the transcription levels of fibrosis-related genes (COLA1A1, αSMA, and TGF-β) in the kidney. These results suggest that renal failure and fibrosis were induced by chronic heat exposure in laying hens. In addition, chronic heat exposure decreased ATP levels and mitochondrial DNA copy number (mtDNA-CN) in renal tissue, suggesting that renal mitochondrial dysfunction occurs under conditions of heat stress. Damaged mitochondria leak mtDNAs into the cytosol and mtDNA leakage may activate the cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) signaling pathway. Our results showed that chronic heat exposure activated the cGAS-STING pathway as indicated by increased expression of MDA5, STING, IRF7, MAVS, and NF-κB levels. Furthermore, the expression of pro-inflammatory cytokines (IL-12) and chemokines (CCL4 and CCL20) was upregulated in heat-stressed hens.ConclusionsThese results suggest that chronic heat exposure induces renal fibrosis and mitochondrial damage in laying hens. Mitochondrial damage by heat stress may activate the mtDNA-cGAS-STING signaling and cause subsequent inflammation, which contributes to the progression of renal fibrosis and dysfunction.