Abstract

The study aims to assess the impact of age, pituitary pars intermedia dysfunction (PPID) and insulin dysregulation (ID) in horses on selected oxidative stress markers. The study includes 32 horses, divided into three groups: “young” adult group (aged 8–16 years old) “geriatric” group (aged 18–24 years old) and the “PPID” group (aged 15–31 years old). The PPID group was further divided into two subgroups: PPID ID+ and PPID ID− based on presence or absence of ID. We measured serum antioxidant stress markers in all horses: total oxidant status (TOS), total antioxidant capacity (TAC), ceruloplasmin (CER), lipofuscin (LPS), malondialdehyde (MDA) and thiols concentrations (containing sulfhydryl group -SH) as well as enzymatic systems: total superoxide dismutase (SOD), cytoplasmic SOD (CuZnSOD), mitochondrial SOD activity (MnSOD). Total serum thiols were significantly lower in the geriatric group and in the PPID group compared to the young group. The MnSOD concentration was higher in the PPID ID+ group compared to the PPID ID−. LPS and MDA concentrations were lower in the PPID ID+ group compared to the PPID ID− group. In the selected study groups of horses, older age, the presence of PPID and ID in the case of PPID had no effect on the studied oxidative stress markers.

Highlights

  • The mechanism of aging and the development of age-related neurodegenerative diseases in humans and animals are associated with the occurrence of oxidative stress and the action of oxygen free radicals [1,2]

  • Stimulation test, resting insulin and insulin after oral sugar test (OST) were within reference intervals

  • We have, for the first time, shown that (i) older age is negatively correlated with serum thiols concentrations in horses; (ii) the presence of pituitary pars intermedia dysfunction (PPID) did not change the status of antioxidative stress markers significantly; (iii) the presence of insulin dysregulation (ID) in PPID horses does not detectably influence the cellular defense against ROS

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Summary

Introduction

The mechanism of aging and the development of age-related neurodegenerative diseases in humans and animals are associated with the occurrence of oxidative stress and the action of oxygen free radicals [1,2]. Age-related changes, as well as oxidative stress, may potentially lead to increased degeneration of the dopaminergic neurons of the hypothalamus [10] This may result in inhibits of dopamine releasing from the hypothalamus terminal nerve, which results in overproduction of the pituitary gland’s intermediate lobe hormones [10]. These degenerative changes induce cells hyperplasia and formation of micro- and macroadenomas in the pars intermedia, which results in excessive proopiomelanocortin production (POMC) and its derivatives such as adrenocorticotropin hormone (ACTH), α-melanocyte stimulating hormone (α-MSH) and β-endorphin [10]. In studies on the impact of oxidative disorders on the occurrence of PPID, mitochondrial SOD (MnSOD)

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