Background: Negative energy balance during late pregnancy in ewes is an important cause of hyperketonemia. Ketone bodies can generate superoxide radicals and cause oxidative stress and cellular dysfunction, as noted in cows with subclinical ketosis or in diabetic people.
Objective: The aim of this study was to evaluate the role of hyperketonemia in initiating the process of lipid peroxidation.
Methods: The study included 10 pregnant ewes (aged 3.5–6 years) with pregnancy toxemia, 10 clinically healthy pregnant ewes, and 10 clinically healthy nonpregnant ewes. Serum concentrations of β-hydroxybutyrate (BHB), cortisol, and glucose, plasma activities of glutathione peroxidase, superoxide dismutase, and catalase, and plasma concentrations of thiobarbituric acid reactive substances (TBARS), markers of lipid peroxidation, and reduced glutathione were measured. Data from the 3 groups were statistically analyzed and compared.
Results: Serum concentrations of BHB, cortisol, and TBARS were significantly higher in ewes with pregnancy toxemia when compared with concentrations in healthy pregnant and nonpregnant groups (P≤.05). In ewes with pregnancy toxemia, a strong positive correlation was found between concentrations of TBARS and BHB (r=.80; P=.002) and between concentrations of BHB and cortisol (r=.76; P=.005).
Conclusions: Oxidative stress and lipid peroxidation are involved in the development and complications of pregnancy toxemia. An association between hyperketonemia and the products of lipid peroxidation has also been demonstrated, suggesting that ketosis is a risk factor in the development of lipid peroxidation and oxidative stress in ewes affected by pregnancy toxemia.