Effect of Excess Dietary Iron on Lipid Composition of Calf Liver, Heart, and Skeletal Muscle

Abstract

Effect of excess dietary iron on lipid composition of calf liver, skeletal muscle, and heart was assessed. High dietary iron (5000 versus 100 ppm in milk replacer DM) had no effect on the relative proportion of lipid classes in liver or their unsaturated fatty acid composition. In muscle some minor lipid components were reduced and cholesterol and sphingomyelin increased. Excessive iron had a marked effect, however, on heart lipid composition, reducing total lipids and almost all lipid classes; triglycerides, sphingomyelin, and lysophosphatidylcholine were increased. Characteristically, sphingomyelin increases in cell membranes in response to aging and numerous pathological conditions. High dietary iron reduced linolenic acid in phosphatidyl-ethanolamine and phosphatidylcholine of both skeletal and cardiac muscle. This may have resulted from iron-caused ethane production from autoxidation of linolenic acid or other n-3 family fatty acids, an effect known to occur in the rat. Linoleic and arachidonic fatty acids appeared to be unaffected. Plasmalogens in muscle and heart phosphatidylethanolamine and phosphatidylcholine were increased by high iron intake. As these alk-1-enyl ethers protect cells from oxidation and radiation damage, their synthesis may have been increased in response to stress from excessive iron. The results indicate that a relatively high concentration of vitamin E may be required in calf milk replacer when excessive iron is present.

A delicate balance: Iron metabolism and diseases of the brain

“…This pathway is not induced by Fenton chemistry; rather it is related with iron-dependent enzymatic activities (Dixon et al, 2012). Indeed, inappropriate intracellular iron accumulation potentially damages a number of proteins such as Ca 2 + -ATPase (Kaplan et al, 1997; Moreau et al, 1998), glutamate transporter (Gnana-Prakasam et al, 2009; Yu et al, 2009; Mitchell et al, 2011), Na + /K + -ATPase (Kaplan et al, 1997; Strugatsky et al, 2003), and N -methyl- D -aspartate (NMDA) receptor (Nakamichi et al, 2002; Munoz et al, 2011), as well as oxidizes lipid such as cholesterol (Kraml et al, 2005; Graham et al, 2010; Shinkyo and Guengerich, 2011), ceramides (Yurkova et al, 2005), and sphingomyelin (Jenkins and Kramer, 1988; Isaac et al, 2006); all of which were proposed to ultimately cause synaptic dysfunction and neuronal cell death (Mattson, 2004). …”

Super-dosing phytase improves the growth performance of weaner pigs fed a low iron diet

“…In the body, unbound Fe is considered cytotoxic owing to its ability to catalyse the production of cell damaging reactive free radicals via the Fenton reaction (Jenkins and Kramer, 1988). Consequently, most body Fe is found associated with proteins.…”

Biometals and Their Therapeutic Implications in Alzheimer's Disease

“…Neuronal iron deposition causes oxidative stress via the Fenton reaction, which might contribute to elevated oxidative stress observed in the AD brain [109]. Iron-induced oxidative stress has been shown to initiate several apoptotic signaling pathways in neurons [110], and damage proteins such as Ca 2+ -ATPase [111][112][113][114], glutamate transporter [115][116][117], apolipoprotein E [118,119], and Na + /K + -ATPase [111,114,120,121], as well as N-methyl-D-aspartate (NMDA) receptor [122][123][124], and lipids such as cholesterol [125][126][127], ceramides [128,129], and unsaturated fatty acids [130][131][132][133], as well as sphingomyelin [134,135]. Oxidative damage to proteins and lipids by iron can cause synaptic dysfunction and neuronal cell death [136].…”