Selenium and vitamin E together improve intestinal epithelial barrier function and alleviate oxidative stress in heat‐stressed pigs

Abstract

New Findings r What is the central question of this study?Oxidative stress may play a role in compromising intestinal epithelial barrier integrity in pigs subjected to heat stress, but it is unknown whether an increase of dietary antioxidants (selenium and vitamin E) could alleviate gut leakiness in heat-stressed pigs. r What is the main finding and its importance? Levels of dietary selenium (1.0 p.p.m.) and vitamin E (200 IU kg −1 ) greater than those usually recommended for pigs reduced intestinal leakiness caused by heat stress. This finding suggests that oxidative stress plays a role in compromising intestinal epithelial barrier integrity in heat-stressed pigs and also provides a nutritional strategy for mitigating these effects.Heat stress compromises the intestinal epithelial barrier integrity of mammals through mechanisms that may include oxidative stress. Our objective was to test whether dietary supplementation with antioxidants, selenium (Se) and vitamin E (VE), protects intestinal epithelial barrier integrity in heat-stressed pigs. Female growing pigs (n = 48) were randomly assigned to four diets containing from 0.2 p.p.m. Se and 17 IU kg −1 VE (control, National Research Council recommended) to 1.0 p.p.m. Se and 200 IU kg −1 VE for 14 days. Six pigs from each dietary treatment were then exposed to either thermoneutral (20°C) or heat-stress conditions (35°C 09.00-17.00 h and 28°C overnight) for 2 days. Transepithelial electrical resistance and fluorescein isothiocyanate-dextran (4 kDa; FD4) permeability were measured in isolated jejunum and ileum using Ussing chambers. Rectal temperature, respiratory rate and intestinal HSP70 mRNA abundance increased (all P < 0.001), and respiratory alkalosis occurred, suggesting that pigs were heat stressed. Heat stress also increased FD4 permeability and decreased transepithelial electrical resistance (both P < 0.01). These changes were associated with changes indicative of oxidative stress, a decreased glutathione peroxidase (GPX) activity and an increased glutathione disulfide (GSSG)-to-glutathione (GSH) ratio (both P < 0.05). With increasing dosage of Se and VE, GPX-2 mRNA (P = 0.003) and GPX activity (P = 0.049) F. Liu and others increased linearly, the GSSG:GSH ratio decreased linearly (P = 0.037), and the impacts of heat stress on intestinal barrier function were reduced (P < 0.05 for both transepithelial electrical resistance and FD4 permeability). In conclusion, in pigs an increase of dietary Se and VE mitigated the impacts of heat stress on intestinal barrier integrity, associated with a reduction in oxidative stress.

Protective effects of resveratrol against high ambient temperature‐induced spleen dysplasia in broilers through modulating splenic redox status and apoptosis

“…However, numerous environmental factors, including HT, can lead to excessive apoptosis, which has a harmful effect on human and animal health. Previous studies indicated that ROS acted as an upstream molecule in the mitochondrial apoptotic pathway, and HT‐induced oxidative stress could cause apoptosis in the small intestine . Oxidative stress may therefore be the intermediate for HT‐induced excessive apoptosis and organ injury.…”

“…Previous studies indicated that ROS acted as an upstream molecule in the mitochondrial apoptotic pathway, [12][13][14] and HT-induced oxidative stress could cause apoptosis in the small intestine. 15,16 Oxidative stress may therefore be the intermediate for HT-induced excessive apoptosis and organ injury. Although numerous studies reported that the HT effect led to oxidative stress in muscle 2,9,10 and intestine, 17 whether this issue occurred in the immune organ was still not known for certain and needed to be investigated.…”

Feeding and nutrition management of heat-stressed dairy ruminants

“…An improved resistance against HS in pigs supplemented with selenium and vitamin E was reported in the review of Renaudeau et al (2012). More recently, Liu et al (2016), in a study carried out on pig, demonstrated that the increase of dietary vitamin E and Se was able to reduce the negative impact of HS on intestinal barrier integrity.…”

Heat stress induces intestinal injury through lysosome- and mitochondria-dependent pathwayin vivoandin vitro

“…The reduction in gastrointestinal blood flow greatly impairs the epithelial cells of the small intestinal villi and induces excessive apoptosis [5, 10, 11]. Recently, studies in multiple animal models have detected heat stress-induced apoptosis in small intestinal tissue and intestinal epithelial cells [5, 12–14]. However, little is known about the biological mechanisms involved in heat stress-induced apoptosis in the small intestine.…”

“…The increase in free radicals from ischemia can lead to ROS-related damage of the intestinal mucosa. Heat stress-related oxidative stress has been shown to cause apoptosis in the small intestines of both rats and pigs [5, 13, 14]. Therefore, oxidative stress may be the intermediate through which heat stress induces intestinal damage and may act upstream of apoptosis.…”