Abstract

BackgroundA better comprehension of the redox status during the periparturient period may facilitate the development of management and nutritional solutions to prevent subclinical hyperketonemia (SCHK) and subclinical hypocalcemia (SCHC) in dairy goats. We aimed to evaluate the variation in the redox status of dairy goats with SCHK and SCHC during their periparturient periods. Guanzhong dairy goats (n = 30) were assigned to SCHK (n = 10), SCHC (n = 10), and healthy (HEAL, n = 10) groups based on their blood β-hydroxybutyrate (BHBA) and calcium (Ca) concentrations. Blood were withdrawn from goats every week from 3 weeks before the expected parturition date to 3 weeks post-kidding. On the same day, the body condition scores (BCS) were evaluated, and the milk yield was recorded for each goat. The metabolic profile parameters and the indicators of oxidative status were determined by using the standard biochemical techniques.ResultsIn comparison with the HEAL goats, SCHK and SCHC goats presented with a more dramatic decline of BCS post-kidding and a significant decrease in the milk yield at 2- and 3-weeks postpartum, ignoring the obvious increase at 1-week postpartum. The levels of non-esterified fatty acids (NEFA) peaked at parturition, exhibiting significantly higher levels from 1-week prepartum to the parturition day in the SCHK and SCHC groups. The malondialdehyde (MDA) concentration was increased in the SCHK goats from 1-week antepartum until 3-weeks postpartum, with its concentration being significantly higher in the SCHC goats at parturition. The hydrogen peroxide (H2O2) concentration was significantly lower in the SCHK and SCHC goats from 2-weeks antepartum to 1-week post-kidding. The total antioxidant capacity (T-AOC) and the superoxide dismutase (SOD) level were decreased at 1-week antepartum in the SCHK and SCHC goats, respectively. The glutathione peroxidase (GSH-Px) level was increased in the SCHK and SCHC goats during the early lactation period.ConclusionsThe SCHK and SCHC goats exerted more efforts to maintain their redox homeostasis and to ensure the production performance than the HEAL goats during their periparturient period, probably owing to more intense fat mobilization and lipid peroxidation in the former.

Highlights

  • A better comprehension of the redox status during the periparturient period may facilitate the development of management and nutritional solutions to prevent subclinical hyperketonemia (SCHK) and subclinical hypocalcemia (SCHC) in dairy goats

  • The milk yield increased with the onset of lactation, and it was higher in the SCHK and SCHC goats at 1-week post-kidding in comparison to that in HEAL goats (P < 0.05), whereas it was significantly lower at 2- (P < 0.05) and 3-weeks (P < 0.01) postpartum in the SCHK and SCHC groups than control group, respectively (Fig. 1B)

  • Values are expressed as means ± standard error of the mean (SEM) from 10 goats/group (n = 10)

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Summary

Introduction

A better comprehension of the redox status during the periparturient period may facilitate the development of management and nutritional solutions to prevent subclinical hyperketonemia (SCHK) and subclinical hypocalcemia (SCHC) in dairy goats. The periparturient period is extremely crucial with respect to maintaining the health and productive performance of dairy goats During this period, the dry matter intake (DMI) often cannot meet the nutrient demands necessary for healthy fetal growth and lactogenesis, resulting in an energy deficit [1, 2]. The dry matter intake (DMI) often cannot meet the nutrient demands necessary for healthy fetal growth and lactogenesis, resulting in an energy deficit [1, 2] Under this condition of metabolic adaptations corresponding to energy deficit, the catabolic pathways of adipose tissues can be triggered; subsequently, the increase in the systemic generation of reactive oxygen species (ROS) that react with every organic molecule they encounter to produce reactive oxygen metabolites (ROMs), including superoxide anions (O2−), hydroxyl radicals (·OH), and hydrogen peroxide (H2O2) [3,4,5]. Malondialdehyde (MDA), an end-product of ROSinduced lipoperoxidation, can induce oxidative damage and cytotoxicity by attacking cellular macromolecules (such as proteins and nucleic acids) [6]. Accumulating evidence suggests that oxidative stress influences the pathogenesis of several metabolic disorders throughout the transition period [9,10,11,12]

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