Effects Of Chronic Heat Stress Research Articles

Effects of Chronic Heat Stress on Growth, Apoptosis, Antioxidant Enzymes, Transcriptomic Profiles, and Immune-Related Genes of Hong Kong Catfish (Clarias fuscus).

Chronic heat stress can have detrimental effects on the survival of fish. This study aimed to investigate the impact of prolonged high temperatures on the growth, antioxidant capacity, apoptosis, and transcriptome analysis of Hong Kong catfish (Clarias fuscus). By analyzing the morphological statistics of C. fuscus subjected to chronic high-temperature stress for 30, 60, and 90 days, it was observed that the growth of C. fuscus was inhibited compared to the control group. The experimental group showed a significant decrease in body weight and body length compared to the control group after 60 and 90 days of high-temperature stress (p < 0.05, p < 0.01). A biochemical analysis revealed significant alterations in the activities of three antioxidant enzymes superoxide dismutase activity (SOD); catalase activity (CAT); glutathione peroxidase activity (GPx), the malondialdehyde content (MDA), and the concentrations of serum alkaline phosphatase (ALP); Aspartate aminotransferase (AST); and alanine transaminase (ALT) in the liver. TUNEL staining indicated stronger apoptotic signals in the high-temperature-stress group compared to the control group, suggesting that chronic high-temperature-induced oxidative stress, leading to liver tissue injury and apoptosis. Transcriptome analysis identified a total of 1330 DEGs, with 835 genes being upregulated and 495 genes being downregulated compared to the control group. These genes may be associated with oxidative stress, apoptosis, and immune response. The findings elucidate the growth changes in C. fuscus under chronic high temperature and provide insights into the underlying response mechanisms to a high-temperature environment.

Effects of chronic heat stress on growth performance, liver histology, digestive enzyme activities, and expressions of HSP genes in different populations of Largemouth bass (Micropterus salmoides)

Heat stress has become a significant issue in Largemouth bass (Micropterus salmoides, LMB). Identifying populations with superior heat tolerance abilities contribute to the breeding of new varieties with stress resistance. In this study, three populations of Northern LMB, including “YouLu No.3″ LMB (YL3), wild Northern LMB (NLMB) and Taiwan LMB (TW), as well as one Florida LMB population (M. floridanus, FLMB) were subjected to chronic heat stress. After being exposed to a temperature of 34 ℃ for 60 days, the FLMB group showed the highest final mean body weight (FBW), survival rate (SR), specific growth rate (SGR), and the lowest feed coefficient ratio (FCR) compared to the three Northern LMB groups. The lowest SR was observed in the TW group, while the lowest FBW and SGR, as well as the highest FCR were observed in the NLMB group. The FLMB group showed the lowest damage to the liver, with small focal infiltrations of inflammatory cells. However, the degree of liver damage was gradually worsened in the NLMB, YL3, and TW groups. The NLMB group had a small number of inflammatory cells, while the TW group had more lipid vacuoles and inflammatory cells. The FLMB group exhibited the highest activities of pepsin and lipase, whereas the NLMB group showed the lowest activity of amylase. Compared to the three Northern LMB groups, the FLMB group exhibited higher expressions of HSP60/70 and HSP90aa1/b1. Additionally, the YL3 group exhibited higher expressions of HSP60 and HSP90aa1/b1 compared to the NLMB and TW groups. In conclusion, our results indicated that the FLMB population had better chronic heat tolerance than the Northern LMB populations. Additionally, the YL3 population exhibited superior heat tolerance compared to the TW and NLMB populations. Our study provides valuable information for the future selective breeding of LMB varieties.

Chronic heat stress inhibits glycogen synthesis through gga-miR-212-5p/GYS1 axis in the breast muscle of broilers

Studies have demonstrated that chronic heat stress can accelerate glycolysis, decrease glycogen content in muscle, and affect muscle quality. However, the consequences of chronic heat stress on glycogen synthesis, miRNA expression in pectoralis major (PM) muscle, and its regulatory functions remain unknown. In this study, high-throughput sequencing and cell experiments were used to explore the effects of chronic heat stress on miRNA expression profiles and the regulatory mechanisms of miRNAs in glycogen synthesis under chronic heat stress. In total, 144 cocks were allocated into 3 groups: the normal control (NC) group, the heat stress (HS) group, and the pair-fed (PF) group. In total, 30 differently expressed (DE) miRNAs were screened after excluding the effect of feed intake, which were mainly related to metabolism, signal transduction, cell growth and death. Furthermore, the gga-miR-212-5p/GYS1 axis was predicted to participate in glycogen synthesis through the miRNA-mRNA analysis, and a dual-luciferase reporter test assay confirmed the target relationship. Mechanistically, chronic heat stress up-regulated gga-miR-212-5p, which could inhibit the expression of GYS1 in the PM muscle. Knocking down gga-miR-212-5p alleviates the reduction of glycogen content caused by chronic heat stress; overexpression of gga-miR-212-5p can reduce glycogen content. This study provided another important mechanism for the decreased glycogen contents within the PM muscle of broilers under heat stress, which might contribute to impaired meat quality.

Effects of Chronic Heat Stress on Kidney Damage, Apoptosis, Inflammation, and Heat Shock Proteins of Siberian Sturgeon (Acipenser baerii)

Chronic heat stress caused by global warming can have serious implications for fish survival. The kidney plays a central role in many homeostatic functions, including water and electrolyte regulation. However, there is limited knowledge about the effect of heat stress on fish kidneys. In this study, water temperatures were increased from 20 °C to 24 °C and 28 °C in 8 days at a warming rate of 1 °C/d, and then maintained for 12 days. We investigated the effects of mild heat stress (24 °C) and high heat stress (28 °C) on Siberian Sturgeon (Acipenser baerii) kidneys using histological observation, flow cytometry detection, and RT-qPCR. Our histological observations revealed that heat stress caused significant infiltration of inflammatory cells in the kidney, especially at 28 °C. The flow cytometry assay demonstrated a significant increase in the number of apoptotic cells after heat stress at 28 °C compared to a control group at 20 °C (p = 0.033). The level of plasma creatinine was significantly increased in the 28 °C group compared to the control group (p = 0.001). In addition, the mRNA expression levels of heat shock protein GRP75 increased (p = 0.009). The results indicate that heat stress at 28 °C caused damage to the kidneys of A. baerii and triggered the protective response of heat shock proteins. In conclusion, this study contributes to the understanding of the coping strategies of the kidney of A. baerii for chronic heat stress.

Effects of heat stress on the chemical composition, oxidative stability, muscle metabolism, and meat quality of Nile tilapia (Oreochromis niloticus).

The present study investigated the effects of chronic heat stress (HS) on the chemical composition, oxidative stability, muscle metabolism, and meat quality of Nile tilapia (Oreochromis niloticus). Compared with the control (26°C), chronic HS (32°C) lowered growth performance, the contents of whole-body lipid, muscle protein, and muscle lipid. Also, HS significantly increased the contents of reactive oxygen species (ROS) and decreased antioxidative status, causing a decline in meat quality, including increased lipid and protein oxidation, the centrifugal water loss, and cooking loss as well as decreased the fragmentation index and pH at 24h, which may be attributed to induced apoptosis by excessive ROS in Nile tilapia meat. Moreover, metabolomic analysis showed HS lowered flavor and nutritional value by affecting amino acid, lipid, and nucleotide metabolism. These results reveal that HS adversely affects oxidative stability, meat quality, flavor, and nutrition, warranting its recognition and prevention.

Innate immune and chronic heat stress responses in sturgeons: Advances and insights from studies on Russian sturgeons

Chronic stress deteriorates the immune function of fish, thereby increasing their vulnerability to infections. However, the molecular and cellular mechanisms underlying stress-mediated immunosuppression and infection susceptibility in fish remain largely unknown. Understanding these mechanisms will contribute to improving fish welfare and their farm production. Herein, we review the challenges of sturgeon aquaculture in subtropical countries, where current climate change has giving rise to significant temperature increments during summer. This leads to the exposure of fish to stressful conditions during these months. Chronic heat stress deserves attention considering the rapid warming rate of the planet. It is already affecting wild fish populations, with disastrous consequences for sturgeons, which are one of the most endangered fish species in the world. In this context, we discuss the most recent advances through the studies on the effects of chronic heat stress on the innate immune components of sturgeons. To this end, we summarise the findings of studies focusing on the aquaculture of Russian sturgeons and observations made on other Acipenser species. Special attention is given to acute-phase proteins, as they might be valuable biomarkers of heat stress and infection, with applicability in monitoring the fish health status in farms.

Negative effects of high-temperature stress on gametophyte performance and their consequences for seed reproduction in wild plants

(1) Plant regeneration by seeds is highly sensitive to temperature stress, particularly in the gametophyte stage. However, most of the existing research has focused on one single stage of gametophyte development and/or conducted using cultivated or a very few model species. Thus, it is unclear whether the results of such studies can be applied to natural populations. (2) To fill this gap, we investigated a) the effects of chronic heat stress (CHS; 17 days) at 35/30 °C (moderate stress) and 40/35 °C (severe stress) on gametophyte performance, and b) how these effects translated into seed quantity and quality. We measured six traits related to male (anther length, pollen production and size) and female (ovary length, ovule production, and size) gametophyte performance and leaf chlorophyll fluorescence (Fv/Fm) in four wild Silene species. The ripe seeds of the treated plants were used to measure seed mass and seed production; the seed germination was characterized in terms of germination percentage, speed, and synchrony. (3) Fv/Fm decreased significantly in both heat treatments, confirming a negative effect of CHS on overall plant performance. All male gametophyte traits decreased significantly in both CHS treatments compared to the control. The length and size of the ovary were significantly smaller in the 40/35 °C treatment than in the 35/30 °C treatment and the control, while ovule production decreased significantly in both CHS treatments compared to the control. The negative effects on gametophyte performance translated into significantly fewer seeds in the 35/30 °C and 40/35 °C treatments compared to the control. CHS treatments did not affect the seed mass. The final germination percentage differed weakly significantly between the severe treatment and the control but did not show any negative impacts by heat stress, whereas seed germination was significantly faster in the treated plants, both moderate and severe. Germination synchrony was not affected by heat treatments. (4) The high sensitivity of gametophytes in vascular plants to high-temperature stress implies that climate change-associated heat waves can significantly impact seed reproduction in wild plants. The altered seed quantity could have potential consequences for the long-term survival of the wild plant populations and the performance of the granivores.

Effect of chronic heat stress on the carbonylation of glycolytic enzymes in breast muscle and its correlation with the growth performance of broilers

Chronic heat stress has detrimental effects on the growth performance of broilers, and the potential mechanism is under exploration. In this study, the protein carbonyl modification was introduced to glycolytic enzymes to evaluate its relationship with the growth performance of heat-stressed (HS) broilers. A total of 144 male 28-day-old broilers were assigned to 3 treatments: the normal control group (NC, raised at 22°C with free access to feed and water), the HS group (raised at 32°C with free access to feed and water), and the pair-fed group (PF, raised at 22°C with an amount of feed equal to that consumed by the HS group on a previous day). Results showed that heat stress decreased the average daily growth, increased the feed-to-gain ratio (F/G), decreased breast muscle rate, and increased abdominal fat rate compared with the NC and PF groups (P < 0.05). Higher cloacal temperature and serum creatine kinase activity were found in the HS group than those of the NC and PF groups (P < 0.05). Heat stress increased the contents of carbonyl, advanced glycation end-products, malonaldehyde, and the activities of catalase, glutathione peroxidase, and total antioxidant capacity compared with the NC and PF groups (P < 0.05). Heat stress increased the contents of glucose and lactate, declined the glycogen content, and lowered the relative protein expressions of pyruvate kinase muscle type, lactate dehydrogenase A type (LDHA), and citrate synthase compared to those of the NC group (P < 0.05). In contrast to the NC and PF groups, heat stress intensified the carbonylation levels of phosphoglucomutase 1, triosephosphate isomerase 1, β-enolase, and LDHA, which were positively correlated with the F/G (P < 0.05). These findings demonstrate that heat stress depresses growth performance on account of oxidative stress and glycolysis disorders. It further increases the carbonylation of glycolytic enzymes, which potentially correlates with the F/G by disturbing the mode of energy supply of broilers.

Chronic heat stress induces renal fibrosis and mitochondrial dysfunction in laying hens

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.

Mild heat stress–induced adaptive immune response in blood mononuclear cells and leukocytes from mesenteric lymph nodes of primiparous lactating Holstein cows

Heat stress negatively affects the metabolism and physiology of the bovine gut. However, it is not known whether heat stress induces an inflammatory response in mesenteric lymph nodes (MLN), the primary origin of gut immune cells, and thus contributes to inflammatory processes in the circulation. Therefore, our objective was to elucidate the effects of chronic heat stress on the systemic activation of acute-phase response in blood, proinflammatory cytokine production in peripheral blood mononuclear cells (PBMC), and the activation of the toll-like receptor signaling (TLR) 2/4 pathway in MLN leucocytes and their chemokines and chemokine receptor profiles in Holstein cows. Primiparous Holstein cows (n = 30; 169 ± 9 d in milk) were exposed to a temperature-humidity index (THI) of 60 [16°C, 63% relative humidity (RH)] for 6 d. Thereafter, cows were evenly assigned to 3 groups: heat-stressed (HS; 28°C, 50% RH, THI = 76), control (CON; 16°C, 69% RH, THI = 60), or pair-feeding (PF; 16°C, 69% RH, THI = 60) for 7 d. On d 6, PBMC were isolated and on d 7 MLN. Plasma haptoglobin, TNFα, and IFNγ concentrations increased more in HS than CON cows. Concomitantly, TNFA mRNA abundance was higher in PBMC and MLN leucocytes of HS than PF cows, whereas IFNG mRNA abundance tended to be higher in MLN leucocytes of HS than PF cows, but not for chemokines (CCL20, CCL25) or chemokine receptors (ITGB7, CCR6, CCR7, CCR9). Furthermore, the TLR2 protein expression tended to be more abundant in MLN leucocytes of HS than PF cows. These results suggest that heat stress induced an adaptive immune response in blood, PBMC, and MLN leukocytes involving the acute-phase protein haptoglobin, proinflammatory cytokine production, and TLR2 signaling in MLN leucocytes. However, chemokines regulating the leucocyte trafficking between MLN and gut seem not to be involved in the adaptive immune response to heat stress.

Effects and potential mechanism of dietary vitamin C supplementation on hepatic lipid metabolism in growing laying hens under chronic heat stress.

The adverse effects of chronic heat stress (CHS)-induced fatty liver syndrome (FLS) on laying hens during the egg-producing stages have been wildly documented. However, until nowadays, the CHS responses of growing laying hens as well as its alleviating effects of vitamin C is rarely reported. In this study, 12-week-old laying hens were subjected to CHS at 36 °C for 10h/d for 3 weeks with or without dietary supplementation of 300mg/kg vitamin C. Results showed that CHS significantly impaired the growth performances and the liver functions of birds, as characterized by reduced feed intake and body weight, increased hepatic lipid accumulation and serum concentrations of TG, ALT and AST, as well as the abnormal expression patterns of the lipid metabolism-related genes. Vitamin C supplementation successfully mitigated the lipid accumulation, while showed no alleviating effect on the serum contents of ALT or AST, which are two key indicators of the liver functions. Metabolomic analysis based on UPLC-Q-TOF/MS identified 173 differential metabolites from the HS and HSV group samples, and they are mainly enriched in the pathways related to the cellular components, vitamin and amino acid metabolism and the energy substance metabolism. The results indicate that CHS-induced hepatic lipid deposition in growing laying hens is effectively alleviated by dietary supplementation of vitamin C, which is probably resulted from the alterations of hepatocellular metabolic patterns.

Effects of chronic heat stress on the immunophenotyping of lymphocytes in immune organs of growing pigs.

This study aimed to investigate the effects of chronic heat stress on the immunophenotyping of lymphocytes in immune organs of growing pigs. A single-factor randomized block design was used, and 15 healthy growing large white barrows (5 litters, 3 pigs/litter) with similar body weight (40.8 kg) were assigned into 3 groups (5 pigs in each group). Groups were: control group (Con, in 23 °C environmental control chamber, fed ad libitum), heat stress group (HS, in 33 °C environmental control chamber, fed ad libitum), and pair-fed group (PF, in 23 °C environmental control chamber, fed diets according to the feed intake of HS group). After a 7-d adaption, the experiment lasted for 21 d. The results showed as follows: (1) activated T cells in the thymus of HS pigs were higher than those in PF pigs (P < 0.05). Monocytes and dendritic cells in the thymus of HS pigs were significantly higher than that in Con and PF pigs (P < 0.05), while the proportions of these 2 lymphocytes in the thymus of Con pigs did not differ from PF pigs (P > 0.05). Compared with Con pigs, the proportion of CD4+ (P < 0.05) and CD8+ T cells (P < 0.10) in the thymus was increased in HS pigs, while the proportion of CD4+ and CD8+ T cells in PF pigs did not differ from Con pigs (P > 0.05). (2) Compared with Con pigs, significantly decreased T cells, increased B cells and monocytes were found in the spleen of pigs exposed to heat stress (P < 0.05); the proportions of these 3 types of lymphocytes were not significantly different between Con and PF pigs (P > 0.05). The proportions of CD4+ T cells and Treg cells in the spleen of pigs exposed to heat stress tended to be lower than those in the Con pigs (P < 0.10). (3) The proportion of lymphocytes in the tonsils of pigs exposed to heat stress did not differ from Con pigs (P > 0.05); compared with PF pigs, the proportion of Treg cells was significantly decreased in HS pigs (P < 0.05). In conclusion, chronic heat stress stimulates the development and maturation of T cells in the pig thymus toward CD4+ and CD8+ T cells and increases the proportion of monocytes and dendritic cells; under the condition of chronic heat stress, the immune response process in the spleen of pigs is enhanced, but chronic heat stress impairs the survival of CD4+ T cells in the spleen.

Transcriptome analysis reveals the mechanism of chronic heat stress on meat quality of broilers

BackgroundChronic heat stress has a negative impact on poultry meat quality. Although this has been extensively investigated, previous studies have primarily focused on metabolic alterations and oxidative stress in the pectoralis major (PM) muscle under chronic heat stress, and not all of the underlying molecular mechanisms are completely understood.MethodsA total of 144 male Arbor Acres broilers (28 d old) were randomly allocated into 3 treatment groups: (1) the normal control (NC) group, with broilers raised at 22 °C and fed a basal diet; (2) the heat stress (HS) group, with birds raised at 32 °C and fed a basal diet; and (3) the pair-fed (PF) group, with birds raised at 22 °C and fed the amount of feed equal to the feed consumed on the previous day by the HS group. The experiment lasted for 14 d.ResultsChronic heat stress decreased the average daily feed intake and average daily gain, increased feed:gain ratio (P < 0.05); and increased drip loss, cooking loss, shear force, hardness, and decreased pH, redness (a*); and springiness of PM muscle (P < 0.05). Furthermore, chronic heat stress decreased muscle fiber density, increased connective tissue, and led to intracellular vacuolation. The transcriptome analyses indicated that the effect of chronic heat stress on meat quality was not only related to metabolism and oxidative stress, but also to signal transduction, immune system, transport and catabolism, cell growth and death, and muscle structure.ConclusionsChronic heat stress has a negative impact on the growth performance, meat quality, and the PM muscle structure of broilers. Transcriptome analysis revealed a comprehensive understanding of the mechanism of the chronic heat stress-induced deterioration of broiler meat quality at the transcriptional level.

Heat stress in broilers of liver injury effects of heat stress on oxidative stress and autophagy in liver of broilers

This study aimed to investigate the effect of chronic heat stress on oxidative stress in liver of broilers. In our study, chickens were randomly allocated to control 1 group (control 7 d), heat stress 1 group (HS1, 7 d), control 2 group (control 14 d) and heat stress 2 group (HS2, 14 d), with 30 replicates in each group. Broilers in heat stress groups exposed 8 h/day heat stress (35 ± 2°C) for 7 or 14 consecutive days, and the rest of time per day were kept at 23 ± 2℃ the same as control group broilers. Growth performance and the liver tissues were collected for histological observation and detection of organ index and liver redox status. The serum indicators (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) related to liver injury were determined. Moreover, Nrf2-related genes and protein expression levels in liver were measured. The results showed that in heat stress group broilers the body weight gain, feed conversion ratio, liver weight, and liver index were decreased, inflammatory cells infiltration in liver, and serum AST level was enhanced, compared with control group broilers. Moreover, the hepatic malondialdehyde (MDA) and superoxide dismutase (SOD) level were increased after 1 wk of heat stress. Nrf2, Sqstm1/p62, HO-1, and NQO1 mRNA expressions in the liver of broilers were decreased by heat stress. P62 and p-p62 protein expressions were significantly up-regulated, but Nrf2 and keap1 protein level was decreased in heat stress group broilers as compared to control group. The mRNA expression levels of Beclin1, LC3-I, LC3-II were down-regulated significantly with heat stress for 1 wk. The mRNA expression level of mTOR up-regulated after 2 wk of heat stress. In conclusion, heat stress induced liver injury of broilers by down-regulating Nrf2-keap1 signaling pathway and autophagy.

Effect of chronic heat stress on gastrointestinal histology and expression of feed intake-regulatory hormones in broiler chickens

Heat stress (HS) dramatically impairs the growth performance of broiler chickens, mainly as a consequence of reduced feed intake due to the loss of appetite. This study was aimed at evaluating the alterations induced by chronic HS conditions on the morphological and morphometric features of the gastrointestinal (GI) tract and on the expression of some enteroendocrine cells (EECs) involved in the regulation of feed intake in chickens. Three hundred male chickens (Ross 308) were divided into two experimental groups and raised either in thermoneutral environment for the whole fattening period (0–41 days) (TNT group) or subjected to chronic HS conditions (30 °C for 24 h/day) from 35 to 41 days (HS group). Samples of proventriculus, duodenum, jejunum and cecum were collected from 24 broilers (12/group). Haematoxylin-eosin was used for the morphometric evaluations, while immunohistochemistry was applied for the evaluation of EECs expressing ghrelin (GHR), cholecystokinin (CCK), neuropeptide Y (NPY), glucagon-like peptide-1 (GLP-1), and serotonin (5-HT). In the proventriculus, HS reduced total wall thickness and mucous layer height (P ≤ 0.01) as well as mean diameter, circumference, and area of the compound tubular glands (P ≤ 0.001) with respect to TNT. The small intestine of HS birds was characterised by decreased villous height and total thickness (duodenum, P ≤ 0.01; jejunum, P ≤ 0.001), whereas crypt depth and width were reduced only in the jejunum (P ≤ 0.01). HS had negligible effects on the morphological aspects of the cecum. In the proventriculus, an increase in GHR and NPY EECs was observed in response to HS (P ≤ 0.001). Similarly, the small intestine villi of the HS group showed greater GLP-1 (P ≤ 0.05), 5-HT (P ≤ 0.001) and CCK (P ≤ 0.01) EECs. Moreover, the expression of 5-HT EECs was higher in the duodenal (P ≤ 0.01) and jejunal (P ≤ 0.01) crypts of HS birds, whereas GLP-1 and CCK EECs increased only in jejunal crypts (P ≤ 0.05). Finally, 5-HT EEC expression was increased in the cecum of HS group (P ≤ 0.01). In conclusion, these outcomes demonstrate that chronic HS induces morphometric alterations not only in the small intestine but also in a key organ such as the proventriculus. Furthermore, HS conditions affect the presence and distribution of EECs, suggesting that some GI peptides and biogenic amine may be implicated in the regulation of appetite and voluntary feed intake in heat-stressed broiler chickens.

Chronic heat stress promotes liver inflammation in broilers via enhancing NF-κB and NLRP3 signaling pathway

BackgroundThis study investigated the effects of chronic heat stress on liver inflammatory injury and its potential mechanisms in broilers. Chickens were randomly assigned to the 1-week control group (Control 1), 1-week heat stress group (HS1), 2-week control group (Control 2), and a 2-week heat stress group (HS2) with 15 replicates per group. Broilers in the heat stress groups were exposed to heat stress (35 ± 2 °C) for 8 h/d for 7 or 14 consecutive days, and the rest of 26 hours/day were kept at 23 ± 2 °C like control group broilers. Growth performance and liver inflammatory injury were examined for the analysis of liver injury.ResultsThe results showed that heat stress for 2 weeks decreased the growth performance, reduced the liver weight (P < 0.05) and liver index (P < 0.05), induced obvious bleeding and necrosis points. Liver histological changes found that the heat stress induced the liver infiltration of neutrophils and lymphocytes in broilers. Serum levels of AST and SOD were enhanced in HS1 (P < 0.01, P < 0.05) and HS2 (P < 0.01, P < 0.05) group, compared with control 1 and 2 group broilers. The MDA content in HS1 group was higher than that of in control 1 group broilers (P < 0.05). Both the gene and protein expression levels of HSP70, TLR4 and NF-κB in the liver were significantly enhanced by heat stress. Furthermore, heat stress obviously enhanced the expression of IL-6, TNF-α, NF-κB P65, IκB and their phosphorylated proteins in the livers of broilers. In addition, heat stress promoted the activation of NLRP3 with increased NLRP3, caspase-1 and IL-1β levels.ConclusionsThese results suggested that heat stress can cause liver inflammation via activation of the TLR4-NF-κB and NLRP3 signaling pathways in broilers. With the extension of heat stress time, the effect of heat stress on the increase of NF-κB and NLRP3 signaling pathways tended to slow down.

Oxidative Stability, Carcass Traits, and Muscle Fatty Acid and Amino Acid Profiles in Heat-Stressed Broiler Chickens.

The objective was to elucidate the effects of chronic heat stress on carcass traits, muscle oxidative stability, muscle fatty acids and amino acid profiles in broiler chickens. A total of 100-day-old male Ross broiler chicks were divided into two equal groups of five replicates. The control group (TN) was maintained on a thermoneutral condition, while the experimental group (HS) was subjected to 8 h of heat stress (34 °C). The HS group showed lower dressing percentage and breast yield compared with the TN group (p = 0.040 and 0.042, respectively). Meanwhile, heat stress significantly increased the percentage of abdominal fat in broiler chickens (p = 0.001). The HS group showed significantly lower levels of PUFA (linoleic, docosahexaenoic and eicosapentaenoic) in the breast (p = 0.003, 0.002 and 0.001, respectively) and thigh (p = 0.001, 0.009 and 0.003, respectively) muscles than did the TN group. The levels of α-lenolinec acid in the breast and thigh muscles did not differ between both experimental groups (p = 0.818 and 0.060, respectively). With exception of threonine, tyrosine and phenylalanine, the levels of essential AA in the breast muscles were significantly (p ˂ 0.05) reduced in the HS group. The HS group showed significantly higher concentration of malondialdehyde (MDA) in the breast muscles (p = 0.032). Meanwhile, the concentration of MDA in the thigh muscles did not differ between both experimental groups (p = 0.149). Furthermore, the HS group showed significantly lower superoxide dismutase and catalase in heart tissues (p = 0.005 and 0.001, respectively). In conclusion, chronic thermal stress deteriorates carcass yield and the oxidative stability of breast muscles, as well as the levels of PUFA and essential AA in broiler chickens. However, the oxidative stability of thigh muscles was not affected.

Antioxidant and anti-apoptotic potential of whole-pomegranate extract promoted growth performance, physiological homeostasis, and meat quality of V-line rabbits under hot summer conditions

The present research evaluated the antioxidant and anti-apoptotic potentialities of whole-pomegranate extract (WPE) on the performance, hemato-biochemical indices, carcass yield, and meat quality of male V-line rabbits under hot summer conditions. For this purpose, 48 weaned, 4-week-old male V-line rabbits were randomly divided into groups of 12 as: group 1 was fed a basal diet (control); and groups 2, 3, and 4 were fed a basal diet supplemented with 1,000 mg/kg (T1), 1,250 mg/kg (T2), and 1,500 mg/kg (T3) of WPE, respectively, for 60 days during the summer. Chromatographic analysis of WPE indicated that syringic acid (SA), vanillic acid and caffeic acid were the predominant flavonoids, while Eicosapentaenoic acid (EPA) was the major quantified fatty acid. Concerning growth performance, WPE supplementation increased the final rabbit weight gain compared with that of the control. Meat-quality traits that were significantly affected (P < 0.05) by dietary WPE supplementation were tenderness and yellowness. Physiologically, WPE induced high levels of dose-dependent hemoglobin, superoxide dismutase (SOD), total antioxidant capacity (TAC), and high-density lipoprotein cholesterol. In addition, WPE significantly restricted heat oxidative stress indicators, namely malondialdehyde, aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol, triacylglycerol, and white blood cells, which were adversely affected by summer heat stress in the control rabbits (P < 0.05). However, there were no significant variations (P> 0.05) in the catalase and creatinine levels between the WPE-treated groups and the control. Genetically, WPE increased the expressions of the antioxidant glutathione peroxidase (GPX1) and anti-apoptotic B-cell lymphoma 2 (Bcl-2) genes and inhibited the expressions of Bcl-2 Associated X-protein (Bax) and caspase-3 genes. The LibDock ligand-protein modelling suggested that the three biological candidates most likely modulated by SA supplementation at the molecular level were catalase enzyme, glutathione peroxidase (GPX1), and caspase genes. Collectively, rabbit supplementation with 1,250 or 1,500 mg/kg WPE potentially protected V-line rabbits from adverse effects of chronic heat stress by improving endogenous and genetic expressions of antioxidant and anti-apoptotic enzymes and genes.

Chronic heat stress affects the photosynthetic apparatus of Solanum lycopersicum L. cv Micro-Tom

Tomato (Solanum lycopersicum L.) is one of the most widely cultivated crops in the world. Tomato is a plant model and the relationship between yield and biotic/abiotic stress has attracted increasing scientific interest. Tomato cultivation under sub-optimal conditions usually negatively impacts growth and development; in particular, heat stress affects several cellular and metabolic processes, such as respiration and photosynthesis. In this work, we studied the effects of chronic heat stress on various cytological and biochemical aspects using the Micro-Tom cultivar as a model. Photosynthetic efficiency decreased during heat stress while levels of post-photosynthetic sugars (sucrose, fructose, glucose and glucose 6-phosphate) oscillated during stress. Similarly, photosynthetic pigments (lutein, chlorophyll a, chlorophyll b and β-carotene) showed an oscillating downward trend with partial recovery during the stress-free phase. The energetic capacity of leaves (e.g. ATP and ADP) was altered, as well as the reactive oxygen species (ROS) profile; the latter increased during stress. Important effects were also found on the accumulation of Rubisco isoforms, which decreased in number. Heat stress also resulted in a decreased accumulation of lipids (oleic and linoleic acid). Photosynthetically alterations were accompanied by cytological changes in leaf structure, particularly in the number of lipid bodies and starch granules. Prolonged heat stress progressively compromised the photosynthetic efficiency of tomato leaves. The present study reports multi-approach information on metabolic and photosynthetic injuries and responses of tomato plants to chronic heat stress, highlighting the plant's ability to adapt to stress.

Effects of thermal manipulation of eggs on the response of jejunal mucosae to posthatch chronic heat stress in broiler chickens

In this study, the aim was to investigate effects of chronic heat stress (CHS) on the mRNA levels of proinflammatory cytokines (interleukin [IL]-6, IL-8, IL-1β, and tumor necrosis factor alpha [TNF-α]), toll-like receptors (TLR2 and TLR4), heat shock proteins (Hsp70, heat shock transcription factor [HSF]-1, and HSF3) and antioxidant enzymes (catalase, glutathione peroxidase, NADPH oxidase, and superoxide-dismutase) in the jejunal mucosae of broiler chickens subjected to thermal manipulation (TM) during embryogenesis. TM was carried out at 39°C and 65% relative humidity (RH) for 18 h daily from embryonic days 10 to 18. Control group was incubated at 37.8°C and 56% RH. CHS was induced by raising the temperature to 35°C for 7 D throughout posthatch days 28 to 35. On post-hatch-day 28 (day zero of CHS) and after 1, 3, 5, and 7 D of CHS, the jejunal mucosae were collected from both groups to evaluate the mRNA levels by real-time reverse transcription-PCR analysis. On day zero of CHS, the mRNA levels of antioxidant enzymes, TLRs, HSF3, IL-1β, and TNF-α were not significantly different between TM and control groups, while the levels of IL-6, IL-8, and HSF1 were lower and the level of Hsp70 was higher in TM. However, during CHS, the mRNA levels of antioxidant enzymes, IL-1β, TNF-α, TLR4, and HSF1 were significantly lower in TM than in controls, while the levels of TLR2 and IL-8 were significantly higher in TM than in controls. In addition, TM led to significant increase of mRNA levels of IL-6 and HSF3 after 1 D and Hsp70 after 3 D of CHS and to significant decrease of mRNA levels of IL-6 after 3 and 5 D, HSF3 after 7 D, and Hsp70 after 5 D of CHS. Results of this study suggest that TM led to altered posthatch antioxidant, immunological, and Hsp response to CHS in the jejunal mucosae of broiler chickens, probably indicating that TM may mitigate the adverse effects of CHS.