Royal jelly protects male rats from heat stress-induced reproductive failure.

Royal jelly (RJ) as an antioxidant has been shown to have attenuated oxidative stress damages in reproductive organs. The objective was carried out the effects of RJ on sperm characteristics, sperm malondialdehyde (MDA) concentration and in vitro fertilisation (IVF) outcome in heat stress (HS) exposed male rats. Forty-eight male rats were randomly divided into eight groups; group 1 received normal saline, group 2 received RJ (100 mg kg-1  day-1 ; PO), groups 3, 4 and 5 were heat-stressed (43, 39 and 37°C for 20 min per day respectively) and groups 6, 7 and 8 were heat-stressed along with RJ (43, 39 and 37°C for 20 min per day, respectively, plus RJ at a dose of 100 mg kg-1  day-1 ; PO). The HS was induced through immersion of experimental rat scrotums in a water bath. After 48 days, the HS induced remarkable diminish in sperm motility, viability and fertilising potential along with reduced blastulation rate and enhanced sperm chromatin abnormality, MDA levels and DNA damage. Nevertheless, RJ co-administration improved sperm characteristics and early embryo development as well as sperm lipid peroxidation level. Our data suggest that RJ can effectively ameliorate the experimental HS-induced infertility in rats through MDA concentration restoration and sperm characteristics and pre-implantation embryo development improvement.

Effects of a short-term supranutritional selenium supplementation on redox balance, physiology and insulin-related metabolism in heat-stressed pigs.

Heat stress (HS) disrupts redox balance and insulin-related metabolism. Supplementation with supranutritional amounts of selenium (Se) may enhance glutathione peroxidase (GPX) activity and reduce oxidative stress, but may trigger insulin resistance. Therefore, the aim of this experiment was to investigate the effects of a short-term high Se supplementation on physiology, oxidative stress and insulin-related metabolism in heat-stressed pigs. Twenty-four gilts were fed either a control (0.20 ppm Se) or a high Se (1.0 ppm Se yeast, HiSe) diet for 2 weeks. Pigs were then housed in thermoneutral (20°C) or HS (35°C) conditions for 8 days. Blood samples were collected to study blood Se and oxidative stress markers. An oral glucose tolerance test (OGTT) was conducted on day 8 of thermal exposure. The HS conditions increased rectal temperature and respiration rate (both p < .001). The HiSe diet increased blood Se by 12% (p < .05) and ameliorated the increase in rectal temperature (p < .05). Heat stress increased oxidative stress as evidenced by a 48% increase in plasma advanced oxidized protein products (AOPPs; p < .05), which may be associated with the reductions in plasma biological antioxidant potential (BAP) and erythrocyte GPX activity (both p < .05). The HiSe diet did not alleviate the reduction in plasma BAP or increase in AOPPs observed during HS, although it tended to increase erythrocyte GPX activity by 13% (p = .068). Without affecting insulin, HS attenuated lipid mobilization, as evidenced by a lower fasting NEFA concentration (p < .05), which was not mitigated by the HiSe diet. The HiSe diet increased insulin AUC, suggesting it potentiated insulin resistance, although this only occurred under TN conditions (p = .066). In summary, HS induced oxidative stress and attenuated lipid mobilization in pigs. The short-term supranutritional Se supplementation alleviated hyperthermia, but did not protect against oxidative stress in heat-stressed pigs.

Coptidis Rhizoma Prevents Heat Stress-Induced Brain Damage and Cognitive Impairment in Mice.

Heat stress conditions lead to neuroinflammation, neuronal death, and memory loss in animals. Coptidis Rhizoma (CR) exhibits potent fever-reducing effects and has been used as an important traditional medicinal herb for treating fever. However, to date, the effects of antipyretic CR on heat-induced brain damages have not been investigated. In this study, CR significantly reduced the elevation of ear and rectal temperatures after exposure to heat in mice. Additionally, CR attenuated hyperthermia-induced stress responses, such as release of cortisol into the blood, and upregulation of heat shock protein and c-Fos in the hypothalamus and hippocampus of mice. The administration of CR inhibited gliosis and neuronal loss induced by thermal stress in the hippocampal CA3 region. Treatment with CR also reduced the heat stress-induced expression of nuclear factor kappa ß, tumor necrosis factor-α, and interleukin-1ß (IL-1ß) in the hippocampus. Moreover, CR significantly decreased proinflammatory mediators such as IL-9 and IL-13 in the heat-stressed hypothalamus. Furthermore, CR attenuated cognitive dysfunction triggered by thermal stress. These results indicate that CR protects the brain against heat stress-mediated brain damage via amelioration of hyperthermia and neuroinflammation in mice, suggesting that fever-reducing CR can attenuate thermal stress-induced neuropathology.

Acute brief heat stress in late gestation alters neonatal calf innate immune functions.

Heat stress, as one of the environmental stressors affecting the dairy industry, compromises the cow milk production, immune function, and reproductive system. However, few studies have looked at how prenatal heat stress (HS) affects the offspring. The objective of this study was to evaluate the effect of HS during late gestation on calf immunity. Calves were born to cows exposed to evaporative cooling (CT) or HS (cyclic 23-35°C) for 1 wk at 3 wk before calving. Both bull and heifer calves (CT, n=10; HS, n=10) were housed in similar environmental temperatures after birth. Both CT and HS calves received 3.78 L of pooled colostrum within 12 h after birth and were fed the same diet throughout the study. In addition to tumor necrosis factor α, IL-1ß, IL-1 receptor antagonist (IL-1RA), and toll-like receptor (TLR)2, and TLR4 mRNA expression, the expression of CD14(+) and CD18(+) cells, and DEC205(+) dendritic cells were determined in whole blood samples at d 0, 3, 7, 14, 21, and 28. The neutrophil to lymphocyte ratio, differential cell counts, and the hematocrit were also determined. During late gestation, the HS cows had greater respiration rates, rectal temperatures, and tended to spend more time standing compared with the CT cows. The HS calves had less expression of tumor necrosis factor-α and TLR2 and greater levels of IL-1ß, IL-1RA, and TLR4 compared with CT calves. The HS calves also had a greater percentage of CD18(+) cells compared with the CT calves. Additionally, a greater percentage of neutrophils and lesser percentage of lymphocytes were in the HS calves compared with the CT calves. The results indicate that biomarkers of calves' immunity are affected in the first several weeks after birth by HS in the dam during late gestation.

Sweat loss during heat stress contributes to subsequent reductions in lower-body negative pressure tolerance.

The contribution of sweating to heat stress-induced reductions in haemorrhagic tolerance is not known. This study tested the hypothesis that fluid loss due to sweating contributes to reductions in simulated haemorrhagic tolerance in conditions of heat stress. Eight subjects (35 ± 8 years old; 77 ± 5 kg) underwent a normothermic time control and two heat stress trials (randomized). The two heat stress trials were as follows: (i) with slow intravenous infusion of lactated Ringer solution sufficient to offset sweat loss (IV trial); or (ii) without intravenous infusion (dehydration; DEH trial). Haemorrhage was simulated via progressive lower-body negative pressure (LBNP) to presyncope after core body (intestinal) temperature was raised by ~1.5 °C using a water-perfused suit or a normothermic time control period. The LBNP tolerance was quantified via a cumulative stress index. Middle cerebral artery blood velocity (transcranial Doppler) and mean blood pressure (Finometer®) were measured continuously. Relative changes in plasma volume were calculated from haematocrit and haemoglobin. Increases in core body temperature and sweat loss (~1.6% body mass deficit) were similar (P > 0.05) between heat stress trials. Slow intravenous infusion (1.2 ± 0.3 litres) prevented heat-induced reductions in plasma volume (IV trial, -0.6 ± 6.1%; and DEH trial, -6.6 ± 5.1%; P = 0.01). Intravenous infusion improved LBNP tolerance (632 ± 64 mmHg min) by ~20% when compared with the DEH trial (407 ± 117 mmHg min; P = 0.01), yet tolerance remained 44% lower in the IV trial relative to the time control normothermic trial (1138 ± 183 mmHg min; P < 0.01). These data indicate that although sweat-induced dehydration impairs simulated haemorrhagic tolerance, this impairment is secondary to the negative impact of heat stress itself.

Elevated local skin temperature impairs cutaneous vasoconstrictor responses to a simulated haemorrhagic challenge while heat stressed.

During a simulated haemorrhagic challenge, syncopal symptoms develop sooner when individuals are hyperthermic relative to normothermic. This is due, in part, to a large displacement of blood to the cutaneous circulation during hyperthermia, coupled with inadequate cutaneous vasoconstriction during the hypotensive challenge. The influence of local skin temperature on these cutaneous vasoconstrictor responses is unclear. This project tested the hypothesis that local skin temperature modulates cutaneous vasoconstriction during simulated haemorrhage in hyperthermic humans. Eight healthy participants (four men and four women; 32 ± 7 years old; 75.2 ± 10.8 kg) underwent lower-body negative pressure to presyncope while heat stressed via a water-perfused suit sufficiently to increase core temperature by 1.2 ± 0.2 °C. At forearm skin sites distal to the water-perfused suit, local skin temperature was either 35.2 ± 0.6 (mild heating) or 38.2 ± 0.2 °C (moderate heating) throughout heat stress and lower-body negative pressure, and remained at these temperatures until presyncope. The reduction in cutaneous vascular conductance during the final 90 s of lower-body negative pressure, relative to heat-stress baseline, was greatest at the mildly heated site (-10 ± 15% reduction) relative to the moderately heated site (-2 ± 12%; P = 0.05 for the magnitude of the reduction in cutaneous vascular conductance between sites), because vasoconstriction at the moderately heated site was either absent or negligible. In hyperthermic individuals, the extent of cutaneous vasoconstriction during a simulated haemorrhage can be modulated by local skin temperature. In situations where skin temperature is at least 38 °C, as is the case in soldiers operating in warm climatic conditions, a haemorrhagic insult is unlikely to be accompanied by cutaneous vasoconstriction.

Heat acclimation does not reduce the impact of hyperthermia on central fatigue.

We tested the hypothesis that improved physiological symptoms of passively induced heat acclimation (HA) might impair the impact of hyperthermia on central fatigue and consequently cause greater peripheral fatigue. Subjects in the experimental group (7 males and 6 females) completed seven sessions of HA involving passive heating of the lower body by immersion up to the waist in a water bath at approximately 44 degrees C (air T 23 degrees C, rh 40%) for 45 min, repeated every other day for 2 weeks. During the first and the last HA sessions, participants performed a 2-min MVC of the knee extensors. A TT100 Hz was superimposed on the contraction at about 3, 14, 29, 44, 59, 74, 89, 104, and 119 s. At about 30, 60, 90, and 120 s, the knee extensors were relaxed for 2-3 s and a control TT100 Hz was delivered. The participants in the control group (6 males and 6 females) followed the same exercise protocol on days 1 and 14 in a thermoneutral condition. Peak torque and the muscle voluntary activation and half-relaxation time were assessed during the exercise. The attainment of HA was confirmed by significant decreases in the resting and final rectal temperatures (approximately 0.3 degrees C), heart rate, and physiological stress index, and increased sweating capacity. Lower-body heating resulted in greater central and peripheral fatigue when compared with the thermoneutral condition during the 2-min MVC. Following HA, central and peripheral fatigues were unchanged. We conclude that passively induced HA for 2 weeks improved the physiological symptoms, but did not change central or peripheral fatigue during exercise in hyperthermia.