The impact of Zearalenone on heat-stressed skeletal muscle in pigs.

Heat stress (HS) and Zearalenone (ZEN) exposure affect growth, production efficiency, and animal welfare; and, under extreme situations, both can be lethal. Given that both HS and ZEN independently cause oxidative stress, we hypothesized that simultaneous exposure to HS and ZEN would cause greater oxidative stress in porcine skeletal muscle than either condition, alone. To address this hypothesis, crossbred, prepubertal gilts were treated with either vehicle control (cookie dough) or ZEN (40 µg/kg) and exposed to either thermoneutral (TN; 21.0 °C) or 12-h diurnal HS conditions (night: 32.2 °C; day: 35.0 °C) for 7 d. Pigs were euthanized immediately following the environmental challenge and the glycolytic (STW) and oxidative (STR) portions of the semitendinosus muscle were collected for analysis. In STR, malondialdehyde (MDA) concentration, a marker of oxidative stress, tended to increase following ZEN exposure (P = 0.08). HS increased CAT (P = 0.019) and SOD1 (P = 0.049) protein abundance, while ZEN decreased GPX1 protein abundance (P = 0.064) and activity (P = 0.036). In STR, HS did not alter protein expression of HSP27, HSP70, or HSP90. Conversely, in STW, MDA-modified proteins remained similar between all groups. Consistent with STR, ZEN decreased GPX1 (P = 0.046) protein abundance in STW. In STW, ZEN decreased protein abundance of HSP27 (P = 0.032) and pHSP27 (P = 0.0068), while HS increased protein expression of HSP70 (P = 0.04) and HSP90 (P = 0.041). These data suggest a muscle fiber type-specific response to HS or ZEN exposure, potentially rendering STR more susceptible to HS- and/or ZEN-induced oxidative stress, however, the combination of HS and ZEN did not augment oxidative stress.

Heat stress (HS) and Zearalenone (ZEN), a toxic feed contaminant, affect growth, production efficiency, and animal welfare, and can cause death. As HS and ZEN independently increase oxidative stress, an imbalance of free radical production and clearance, and the likelihood of ZEN contamination during heat events, we hypothesized concomitant exposure would induce oxidative stress in pig skeletal muscle more than either agent alone. To address this, female pigs were treated with a placebo or low dose of ZEN and exposed to ambient temperature or a mild cyclic HS designed to mimic environmental conditions (hot days, cooler nights) for 7 d. Following these treatments, fast- and slow-twitch muscles were collected for analysis. In slow-twitch muscle, we observed increased markers of oxidative stress in pigs exposed to ZEN primarily driven by HS and ZEN treated pigs. Additionally, ZEN reduced antioxidant abundance and enzymatic activity regardless of the environment. Conversely, HS and/or ZEN did not cause oxidative stress in fast-twitch muscle, although ZEN altered antioxidant abundance. Although a mild HS and ZEN dose was used, oxidative stress markers were altered, suggesting that slow-twitch muscle is susceptible to HS- and ZEN-mediated changes. These data raise the possibility that more severe HS exposures and higher ZEN doses may compromise muscle health.

Effects of heat stress during porcine reproductive and respiratory syndrome virus infection on metabolic responses in growing pigs.

Heat stress (HS) and immune challenges negatively impact nutrient allocation and metabolism in swine, especially due to elevated heat load. In order to assess the effects of HS during Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection on metabolism, 9-wk old crossbred barrows were individually housed, fed ad libitum, divided into four treatments: thermo-neutral (TN), thermo-neutral PRRSV infected (TP), HS, and HS PRRSV infected (HP), and subjected to two experimental phases. Phase 1 occurred in TN conditions (22 °C) where half the animals were infected with PRRS virus (n = 12), while the other half (n = 11) remained uninfected. Phase 2 began, after 10 d with half of the uninfected (n = 6) and infected groups (n = 6) transported to heated rooms (35 °C) for 3 d of continuous heat, while the rest remained in TN conditions. Blood samples were collected prior to each phase and at trial completion before sacrifice. PPRS viral load indicated only infected animals were infected. Individual rectal temperature (Tr), respiration rates (RR), and feed intakes (FI) were determined daily. Pigs exposed to either challenge had an increased Tr, (P < 0.0001) whereas RR increased (P < 0.0001) with HS, compared to TN. ADG and BW decreased with challenges compared to TN, with the greatest loss to HP pigs. Markers of muscle degradation such as creatine kinase, creatinine, and urea nitrogen were elevated during challenges. Blood glucose levels tended to decrease in HS pigs. HS tended to decrease white blood cell (WBC) and lymphocytes and increase monocytes and eosinophils during HS. However, neutrophils were significantly increased (P < 0.01) during HP. Metabolic flexibility tended to decrease in PRRS infected pigs as well as HS pigs. Fatty acid oxidation measured by CO2 production decreased in HP pigs. Taken together, these data demonstrate the additive effects of the HP challenge compared to either PRRSV or HS alone.

Effects of mammalian in utero heat stress on adolescent body temperature.

In utero hyperthermia can cause a variety of developmental issues, but how it alters mammalian body temperature during adolescence is not well-understood. Study objectives were to determine the extent to which in utero hyperthermia affects future phenotypic responses to a heat load. Pregnant first parity pigs were exposed to thermal neutral (TN) or heat stress (HS) conditions during the entire gestation. Of the resultant offspring, 12 were housed in TN conditions, and 12 were maintained in HS conditions for 15 days. Adolescent pigs in HS conditions had increased rectal temperature and respiration rate (RR) compared to TN pigs, regardless of gestational treatment. Within the HS environment, no gestational difference in RR was detected; however, GHS pigs had increased rectal temperature compared to GTN pigs. As rectal temperature increased, GTN pigs had a more rapid increase in RR compared to the GHS pigs. Adolescent HS decreased nutrient intake, and body weight gain, but neither variable was statistically influenced by gestational treatments. In summary, in utero HS compromises the future thermoregulatory response to a thermal insult.