Transport stress induces pig jejunum tissue oxidative damage and results in autophagy/mitophagy activation.

Pig transportation is associated with intestinal oxidative stress and results in destruction of intestinal integrity. Autophagy has been contributed to maintain cell homeostasis under stresses. The purpose of this study was to evaluate the effects of transport stress on morphology, intestinal mucosal barrier and autophagy/mitophagy levels in pig jejunum. A total of 16 finishing pigs were randomly divided into two groups. The control group was directly transported to the slaughterhouse and rested for 24 hr. The experimental groups were transported for 5 hr and slaughtered immediately. The results showed that transportation induced obvious stress responses with morphological and histological damage in jejunum accompanying with an elevated level of malondialdehyde (MDA; p < .05), endotoxin (LPS; p < .05), lactic dehydrogenase (LDH; p < .05) and a decreased level of serum superoxide dismutase (SOD; p < .05). Also, hemeoxy genase 1 (HO-1; p < .01) as well as tight junction protein (claudin-1 [p < .001], occludin [p < .05] and zonula occludens 1 [ZO-1; p < 0.05]) levels were attenuated in jejunum tissue, and NADPH oxidase 1 (NOX1; p < .01) mRNA expression was up-regulated. Further research indicated that transport stress could induce autophagy through increasing microtubule-associated protein light chain 3 (LC3; p < .05) and autophagy-related gene 5 (ATG5; p < .01) levels and suppressing p62 expression. Additionally, transport stress increased the protein levels of PTEN-induced putative kinase 1 (PINK1; p < .05) and Parkin (p < .05) which was associated with mitophagy. In conclusions, transport stress could induce the destruction of intestinal integrity and involve in the intestinal mucosal barrier oxidative damage, and also contribute to activation of autophagy/mitophagy.