Plasma and Liver α‐tocopherol in Dairy Cows with Left Abomasal Displacement and Fatty Liver

Abstract

Summary Thirty dairy cows with left abomasal displacement (LAD) and 14 healthy control cows were studied to assess the status of the natural antioxidant vitamin E, lipid peroxidation in the liver (malondialdehyde‐formation) and its relationship to hepatic lipidosis. Blood concentrations of α‐tocopherol, aminotransferase, glutamin dehydrogenase, free fatty acids, β‐hydroxybutyrate and glucose were determined, α‐tocopherol, tryglyceride, glycogen and malondialdehyde (MDA) in wet liver tissue samples were examined. The dietary α‐tocopherol intake and its plasma changes in LDA cows were also investigated. Cows were divided into four groups according to their liver triglyceride contents (< 20; 20–80; > 80 mg/g of fresh tissue; and control groups). The lowest plasma vitamin E and the highest liver vitamin E levels were found in cows with highest hepatic triglyceride content. The highest increase in plasma α‐tocopherol within 5 days was seen in cows with the lowest liver triglyceride (P < 0.01). The liver triglyceride was positively correlated with liver MDA (r = 0.38; P < 0.05) and negatively with plasma α‐tocopherol (r = −0.41; P < 0.01).

Evaluation of oxidative stress, antioxidant status and lipid profile in cattle with displacement of the abomasum

“…Oxidative stress is shown to be involved in the pathogenesis of this disease (10). Many researchers have studied determinations of antioxidant status separately by detection of serum superoxide dismutase, glutathione peroxidase, vitamin E and selenium levels or total antioxidant status in cattle with DA (15,19,22). It is noteworthy that Maden et al (18) recently published results similar to the ones presented in this manuscript on oxidative stress associated with displaced abomasum (i.e.…”

Oxidative stress and antioxidant status in dairy cows during prepartal and postpartal periods

“…Vitamin E neutralizes free radicals by formation of the prooxidant vitamin E radical, which under normal physiological states will be regenerated to vitamin E by GSH-Px and vitamin C. Interestingly, plasma concentrations of vitamin E decrease through the transition period and low antioxidant status is associated with disorders in transition cows (LeBlanc et al 2004). These low concentrations are also associated with increased incidence of fatty liver and displaced abomasums (Mudron et al 1997). Supplementing vitamin E in the pre partum period improves the antioxidant status, decreases inflammatory cytokine production, the incidence and severity of clinical mastitis.…”

Hepatic Oxidative Stress: Role of Liver Biopsy

“…The decrease in hepatic GSH-Px activity in severe fatty degeneration, for example, results in the increase H 2 O 2 (Abd Ellah et al, 2004), which can initiate free radical formation through Fenton's reaction. In addition, the decrease in hepatic vitamin E level, which is an important chainbreaking antioxidant, results in lipid peroxidation and failure to regenerate the ascorbic acid (Mudroň et al, 1997(Mudroň et al, , 1999. Increased hepatic oxidative stress was also reported in cows suffering from glycogen degeneration (Abd Ellah et al, 2004), sawdust liver and liver abscesses (Spolarics, 1999;Abd Ellah et al, 2002;Sayed et al, 2003).…”

“…Examples include, measuring hepatic G6PD activity in chemically induced hepatocellular carcinoma in rat liver (De Jong et al, 2001), and in liver of rat with macronodular cirrhosis induced by long-term thioacetamide administration (Sanz et al, 1997). In cattle, hepatic GSH-Px activity (Abd Ellah et al, 2004) and vitamin E (Mudroň et al, 1997(Mudroň et al, , 1999 were measured in cows suffered from severe fatty degeneration. In addition, hepatic GSH-Px and G6PD activities were determined in cows suffering from glycogen degeneration (Abd Ellah et al, 2004), sawdust liver and liver abscesses (Khan et al, 1987;Spolarics, 1999;Abd Ellah et al, 2002).…”

“…The involvement of oxidative stress in the pathogenesis of hepatic dysfunction in human (Comporti, 1998;Poli et al,1987;Zern et al, 1990;Poli, 1993;Tsai et al, 1993;De Maria et al, 1996;Gonzalez-Correa et al, 1997;Paradis et al, 1997;Feher et al, 1998;Wallace & Miller, 2000;Spirli et al, 2001;Alpini et al, 2002;Cesaratto et al, 2004;Jabłonowska et al, 2005) and animals (Khan et al, 1987;Mudronň et al, 1997;1999;Spolarics, 1999;Sansinanea et al, 2000;Abd Ellah et al, 2002;, 2007, 2008, 2010 has been investigated for many years. Some of the liver diseases were associated with increase (Farinati et al, 1995;Abd Ellah et al, 2002, 2008 or decrease (Mudroň et al, 1997;Barbaro et al, 1999;Abd Ellah et al, 2004;Videla et al, 2004;Czeczot et al, 2006) antioxidants contents. Usually hepatic antioxidants increased at the beginning of hepatic disease and decreased in severe hepatic injury.…”