The effect of melatonin on the thermoregulatory and behavioural responses of donkeys in an open field subjected to heat and packing stresses

Thermoregulatory, behavioral and productive responses of laying hens supplemented with different types and dosages of phytases raised in a hot environment: An integrative approach.

Thermoregulatory responses in riverinebuffaloes against heat stress: An updated review.

To explore whether there is an interaction between melatonin (MT) and calcium (Ca2+) in regulating heat tolerance of plants, we analyzed the response of endogenous MT and Ca2+ to heat stress, and examined the effect of MT and Ca2+ on the reactive oxygen (ROS) accumulation, antioxidant system, and transcripts of heat shock factor (HSF) and heat shock proteins (HSPs) of cucumber seedlings under high temperature stress. Seedlings were foliar sprayed with 100 μmol·L-1 MT, 10 mmol·L-1 CaCl2, 3 mmol·L-1 ethylene glycol tetraacetic acid (EGTA, Ca2+ chelating agent) +100 μmol·L-1 MT, 0.05 mmol·L-1 chlorpromazine (calmodulin antagonist, CPZ) +100 μmol·L-1 MT, 100 μmol·L-1 p-chlorophenylalanine (p-CPA, inhibitor of MT) +10 mmol·L-1 CaCl2 or deionized water (H2O), respectively. The results showed that both endogenous MT and Ca2+ in cucumber seedlings were induced by high temperature stress. The seedlings treated with exogenous MT showed significant increases in the mRNA expression of calmodulin (CaM), calcium-dependent protein kinase (CDPK5), calcineurin B-like protein (CBL3) and CBL interacting protein kinase (CIPK2) compared with the control at normal temperature. The mRNA levels of tryptophane decarboxylase (TDC), 5-hydroxytryptamine-N-acetyltransferase (SNAT) and N-acetyl-5-hydroxytryptamine methyltransferase (ASMT), key genes of MT biosynthesis and endogenous MT content were also induced by Ca2+ in cucumber seedlings. Exogenous MT and CaCl2 alleviated the heat-induced oxidative damage through increasing antioxidant ability, reducing the accumulation of reactive oxygen species (ROS), and upregulating the mRNA abundances of HSF7, HSP70.1 and HSP70.11, as evidenced by mild thermal damage symptoms, lower heat injury index and electrolyte leakage under heat stress. The positive effect of MT-induced antioxidant capacity and mRNA expression of HSPs was removed by adding EGTA and CPZ in stressed seedlings. Similarly, the mitigating role of Ca2+ in the peroxidation damage to high temperature stress was reversed by p-CPA. These results suggested that both MT and Ca2+ could induce heat tolerance of cucumber seedlings, which had crosstalk in the process of heat stress signal transduction.

Human sweating regulation at rest, evaluating thermal inputs effects on thermoregulatory center and internal hypothalamic and skin temperatures

Identifying traits associated with susceptibility or tolerance to heat stress (HS) is a prerequisite for developing strategies to improve efficient pork production during the summer months. Study objectives were to determine the relationship between the thermoregulatory and production responses to acute HS in pigs. Prepubertal gilts (n = 235; 77.9 ± 1.2 kg BW) were exposed to a thermoneutral (TN) period (P1, 24 h; 21.9 ± 0.5 °C, 62 ± 13% RH; fed ad libitum) followed immediately by a subsequent acute HS period (P2, 24 h; 29.7 ± 1.3 °C, 49 ± 8% RH; fed ad libitum). Rectal temperature (TR), skin temperature (TS), and respiration rate (RR) were monitored and BW and feed intake (FI) were determined. All pigs had increased TR, TS, and RR (0.80 °C, 5.65 °C, and 61.2 bpm, respectively; P < 0.01) and decreased FI and BW (29% and 1.10 kg, respectively; P < 0.01) during P2 compared to P1. Interestingly, body temperature indices did not explain variation in FI during P2 (R2 ≤ 0.02). Further, the percent change in BW during P2 was only marginally explained by each body temperature index (R2 ≤ 0.06) or percent change in FI (R2 = 0.14). During HS, TR was strongly correlated with P1 TR (r = 0.72, P < 0.01), indicating a pig's body temperature during TN conditions predicts the severity of hyperthermia during HS. Additionally, the change in TR (ΔTR, HS TR - TN TR) was larger in pigs retrospectively classified as susceptible (SUS) as compared to tolerant (TOL) pigs (1.05 vs. 0.51 °C, respectively; P < 0.01). In summary, thermoregulatory responses and production variables during acute HS are only marginally related. Further, changes in BW and FI were unexpectedly poorly correlated during acute HS (r = 0.34; P < 0.01). Collectively, suboptimal growth is largely independent on the thermoregulatory response and hypophagia during acute HS. Consequently, incorporating solely body temperature indices into a genetic index is likely insufficient for substantial progress in selecting HS tolerant pigs.

We examined the effects of a single 2.5-mg dose of melatonin on the thermoregulatory and circulatory responses to intermittent exercise at a room temperature of 27.2+/-0.4 degrees C (mean+/-S.D.), a relative humidity of 55+/-3% (mean+/-S.D.), and a light intensity of 200-300 lux. In a double-blind cross-over study, six male participants ingested either melatonin or placebo at 11:45 hr. Participants then rested in a semi-supine position for 75 min and completed an intermittent running protocol for 66 min at alternating intensities of 40, 60 and 80% of maximal oxygen uptake. Rectal and mean skin temperature, heart rate, blood pressure, skin blood flow, subjective alertness and sleepiness, ratings of perceived exertion (RPE) and thermal strain were recorded. No effects of melatonin were found on these variables measured during the resting period (P>0.10). During exercise, melatonin was found to moderate the increase in rectal temperature by approximately 0.25 degrees C (P=0.050) and magnify the increase in skin blood flow (P=0.047). Postexercise systolic blood pressure was 7.8+/-2.5 mmHg (mean+/-S.D.) lower than before the exercise in the melatonin trial; a change which differed significantly to that in the placebo trial (P=0.018). Melatonin did not influence subjective alertness and sleepiness before or after exercise and did not change the responses of mean skin temperature, RPE and thermal strain during the exercise (P>0.10). In summary it is apparent that a 2.5-mg dose of melatonin has hypothermic, but not soporific, effects during 66 min of intermittent exercise performed under moderate heat stress. Whether such effects improve endurance athletic performance in hot conditions remains to be confirmed. Our data also suggest that postexercise systolic hypotension is more marked after ingestion of melatonin.

This study was designed to evaluate the effects of melatonin on rectal temperature (RT), respiratory rate (RR), heat shock protein 70 (HSP 70), growth hormone (GH), chute (CS) and exit scores (ES) in beef calves exposed to heat stress during the summer. A total of twenty (20) eight months old calves divided into 2 groups were used for the study: melatonin group (MEL, n = 10) received 24mg of melatonin, once every 28 days, and control group (CON, n = 10) did not receive any subcutaneous melatonin implant. The effect of melatonin on RT, RR, HSP 70, GH, chute (CS) and ES were evaluated biweekly (Day 0, 14, 28, 42, 56, 70). The mean ambient temperature (AT) 24.00 ± 0.21°C, relative humidity (RH) 81.60 ± 0.76 % and temperature-humidity index (THI) 89.97 ± 0.70 recorded during the study were above the normal range reported for calves. The biweekly fluctuation of weight gain (WG) in MEL were higher than the CON. The mean RT (39.40 ± 0.06°C), RR (62.57 ± 1.15 cpm), CS (1.13 ± 0.04) and ES (1.5 ± 0.09) in the MEL group were lower (P &amp;lt; 0.05) than the corresponding values of 40.10 ± 0.06°C, 71.53 ± 1.59 cpm, 1.40 ± 0.07 and 1.80 ± 0.10 in the CON group. The biweekly variations in RT, RR, CS, ES, HSP 70 were lower (P &amp;lt; 0.05) in the MEL than the CON. Growth hormone concentrations were higher at D56 and 70 in MEL compared to the CON. Our results demonstrated that MEL ameliorates heat stress during the summer by lowering RT, RR, CS, and ES of beef heifers during the study period. In addition, melatonin influenced the biweekly variation in WG, RT, RR, CS, ES, HSP 70 and GH of heifers during the study period.

We studied the effects of acute stress and exogenous melatonin in various doses on the intensity of lipid peroxidation in emotiogenic structures of the brain and liver of rats with different activity in the open field. Stress had no effect on the content of malonic dialdehyde in the hypothalamus, sensorimotor cortex, and liver of active and passive rats receiving physiological saline. The influence of melatonin on malonic dialdehyde content depended on the dose of this substance. The amount of malonic dialdehyde in brain structures (active and passive rats) and liver (active rats) increased after administration of exogenous melatonin in doses of 0.5 and 2 mg/kg, but decreased after treatment with the hormone in a dose of 1 mg/kg. Melatonin in various doses decreased malonic dialdehyde content in the liver of passive rats. The effects of melatonin are partly related to modulation of lipid peroxidation in central and peripheral tissues of the organism.

The understanding of stomatal regulation in climate stress is essential for ensuring resilient crops. The investigation of the stomatal regulation in combined heat and drought stress aimed to link effects of exogenous melatonin on stomatal conductance (gs) and its mechanistic interactions with ABA or ROS signaling. Melatonin-treated and non-treated tomato seedlings were subjected to moderate and severe levels of heat (38°C for one or three days) and drought stress (soil relative water content of 50% or 20%) applied individually and in combination. We measured gs, stomatal anatomy, ABA metabolites and enzymatic ROS scavengers. The stomata in combined stress responded predominantly to heat at soil relative water content (SRWC) = 50% and to drought stress at SRWC = 20%. Drought stress increased ABA levels at severe stress, whereas heat stress caused an accumulation of the conjugated form, ABA glucose ester, at both moderate and severe stress. The melatonin treatment affected gs and the activity of ROS scavenging enzymes but had no effect on ABA levels. The ABA metabolism and conjugation of ABA might play a role in stomatal opening toward high temperatures. We provide evidence that melatonin increases gs in combined heat and drought stress, but the effect is not mediated through ABA signaling.

Effects of melatonin on both thermoregulatory responses and hypothalamic serotonin release were assessed in unanesthetized rats at three different ambient temperatures (Ta). Systemic administration of melatonin (30-120 mg/kg, i.p) caused a decrease in both colonic temperature and hypothalamic serotonin (5-HT) release in rats at both Ta 8 and 22 degrees C. The hypothermia was brought about by a decrease in metabolic rate at Ta 8 degrees C, whereas at Ta 22 degrees C the hypothermia was produced by both a decrease in metabolic rate and an increase in cutaneous temperature. However, in the heat (Ta 31 degrees C), neither thermoregulatory responses nor hypothalamic 5-HT release was affected by the same amount of administered melatonin. The melatonin-induced hypothermia and decreased 5-HT release in the hypothalamus were attenuated by selective depletion of brain 5-HT produced by intracerebroventricular injection of 5,7-dihydroxytryptamine. Furthermore, the melatonin-induced hypothermia was almost completely abolished by treatment with a 5-HT2A receptor agonist (DOI) or a 5-HT1A receptor antagonist [(-)-pindolol]. The data indicate that melatonin potentiates the 5-HT1A receptor activation in the hypothalamus and results in hypothermic effects which can be antagonized by the expected hyperthermic effect of DOI.

Physiological and transcriptome analyses provide new insights into the mechanism mediating the enhanced tolerance of melatonin-treated rhododendron plants to heat stress

Pre- and postnatal heat stress abatement affects dairy calf thermoregulation and performance

Thermoregulatory responses via sympathetic nerve activity during heat stress are absent or impaired in persons with spinal cord injury. However, relationships between their injury years and responses of sweating and cutaneous vasodilation to increased core temperature remained unknown. Six of cervical (CSCI; N=6; level of C5‐7; injury years of 1–22 yrs) and 8 thoraciolumbal (SCI; N=8; Th4‐L1; 1–24 yrs) spinal cord injury persons and 10 healthy subjects (AB; able‐body) were recruited. They wore water‐perfused suits with taking a supine position and 33‐degree C water was perfused into the suits to make a whole body thermoneutral condition, while all devices were applied. After 10‐min measurements during thermoneutral condition, heat stress was performed with infusion of 47‐degree C water until esophageal temperature (thermocouples) increased by 1 degree C. Mean arterial pressure (MAP; the brachial artery; Korotkoff's method), mean skin (Tsk) and local chest temperatures (Tchest; thermocouples), sweat rate (SR; capacitance hygrometry) and skin blood flow (SkBF; laser‐Doppler velocimetry) on the chest. Cutaneous vascular conductance (CVC) were calculated as SkBF divided by MAP. Tsk was about 35 degree C in all groups and increased by 3 degree C. Tchest increased by 1.4 degree C during heat stress. CVC increased by 4 times as baseline in AB, 3 times in SCI during heat stress, but no increase was observed in CSCI. Patterns of SR in all groups were similar to CVC. Maximal response of CVC [control/degrees] was tended to be negatively correlated, but that of SR [mg/cm2/min] was positively correlated with injury years. In conclusion, thermoregulatory responses to increased core temperature were absent in CSCI and impaired in SCI. In SCI, sweating response on the chest, where sympathetic nerve activity is intact, is possibly enhanced to compensate for reduced cutaneous vasodilation with increased injury year.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The objectives of this study were to determine the effects of single or repeated short heat stress (HS) challenges that mimicked summer heat waves on performance and thermoregulatory responses in finishing pigs. A total of 45 crossbred castrated males were tested in three consecutive replicates of 15 pigs. Within each replicate, pigs were assigned to one of five treatments. Pigs in treatment group TTT were maintained in thermoneutral conditions (22 °C) for the entire experiment (45 d). Pigs in treatment group HHH were subjected to an HS challenge (32 °C for 5 d) at 113, 127, and 141 d of age (in experimental periods P1, P2, and P3, respectively). Pigs in treatment groups HTT, THT, and TTH were subjected to the HS challenge at 113, 127, or 141 d of age, respectively. Each 5-d challenge was preceded by a 3-d prechallenge period and followed by a 7-d recovery period. Pigs were housed in individual pens and fed ad libitum. HS significantly reduced average daily feed intake (ADFI) and the average daily gain (ADG). Expressed as a percentage of the performance observed during the prechallenge period, ADFI decreased by 12%, 22%, and 26% and ADG decreased by 12%, 43%, and 72% in the HTT, THT, and TTH groups, respectively. Regardless of the experimental group, no compensatory performance was observed during the recovery period, suggesting that HS has a long-lasting effect on animal performance. Pigs subjected to HS had an immediate increase in core body temperature (Tcore), skin temperature, and respiratory rate, all of which gradually decreased during the HS challenge. Based on Tcore measurements, hypothermia was observed during the recovery period in each of the three experimental periods, especially for pigs in the HHH and the HTT groups but only during the first HS cycle. Repeated exposure to HS for the HHH group resulted in heat acclimation responses characterized by a lower increase in Tcore and lower decrease in ADFI during P2 and P3 than during P1.

During the onset of heat stroke, heat is the most fundamental cause of injury. It has been demonstrated in a number of animal and cell experiments that hyperthermia can directly induce tissue damage and cell death, and cells can activate apoptotic signals or direct necrosis depending on the extent of heat stress. In general, high heat stress activates apoptotic signals and induce apoptosis. Therefore, the form of damage of tissue cells during the onset of heat stroke is currently considered to be mainly apoptosis. In recent years, it has been found that the heat stress molecular biology research regulates the physiological activities of cells in a wide range and participates in the intracellular signal transduction process. Melatonin and its metabolites are broad-spectrum antioxidants and free radical scavengers that regulate a variety of molecular pathways, such as inflammation, proliferation, apoptosis, and metastasis, under different pathophysiological conditions. This article summarized the research on the effects of melatonin and heat shock on apoptosis, and evaluated the possible protective effects of melatonin on the pathogenesis of heat stroke, and provided new therapeutic ideas for the clinic.