Abstract
ABSTRACT Early-life stress has been well studied in humans and laboratory animals; however, the impacts of similar adversity on the welfare of domestic dogs has recently begun to be addressed. For example, associations between processes linked to mitochondrial function, such as oxidative stress (OS) and proinflammatory immune systems, have been under-researched. Yet, mitochondria are targets and mediators of stress pathologies. This study investigates the impact of early-life stress on OS and proinflammatory immune responses in shelter dogs compared to client-owned dogs. We measured OS markers, including total antioxidant capacity (TAC), lipid oxidative damage, catalase (CAT) activity, glutathione peroxidase (GPx) activity, and superoxide dismutase (SOD) concentration, as well as inflammatory cytokines IL-1β, IL-6, and TNF-α. Shelter dogs exhibited significantly higher lipid oxidative damage (p = 0.0265), lower CAT activity (p = 0.002), higher SOD concentration (p < 0.001), and increased IL-1β levels (p = 0.027) compared to client-owned dogs. Compared to client-owned dogs, shelter dogs showed increased OS and inflammation, suggesting higher susceptibility to zoonotic and chronic diseases.
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