title: Impact of iron and vitamin C-containing supplements on preterm human milk: in vitro.
abstract: Stress due to reactive oxygen species (ROS) may lead to neonatal diseases, such as necrotizing enterocolitis and respiratory distress. Enteral supplements for premature infants (PREM) added to human milk (HM) to increase nutrient content may induce lipid oxidation due to free radical formation via Fenton chemistry. We hypothesized that ferrous iron and vitamin C-containing supplements added to HM in vitro cause oxidation of milk fats, affect intracellular redox balance, and induce DNA damage. Lipid peroxidation in HM was measured by FOX-2 and TBARS assays; fatty acid composition of supplemented HM was measured by gas chromatography. Two cell culture bioassays were used for assessing either intracellular oxidative stress or DNA damage: the former involved Caco-2BBe cells, a secondary differentiated cell line, and the latter utilized FHS-74 Int cells, a primary fetal small intestinal culture. Lipid oxidation products of HM increased after the addition of iron alone, iron and vitamin C, or iron and a vitamin C-containing supplement (Trivisol, TVS). A reduced content of mono and polyunsaturated fatty acids in HM was also observed. Iron, not iron+vitamin C, but iron+TVS induced significant intracellular oxidative stress in FHS-74 Int cells. In contrast, iron, either alone or in combination with TVS or vitamin C, increased DNA damage in Caco-2BBE cells. Iron supplementation may increase oxidative stress in PREM infants and should be given separately from vitamin C-containing supplements.
authors: Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada R3T 2N2.
authors: James K
authors: JK
authors: Friel
authors: William L
authors: WL
authors: Diehl-Jones
authors: Miyoung
authors: M
authors: Suh
authors: Apollinaire
authors: A
authors: Tsopmo
authors: Vaibhav P
authors: VP
authors: Shirwadkar
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000328:Adult; D000906:Antibodies / Q000276:immunology; D000975:Antioxidants / Q000032:analysis; D001205:Ascorbic Acid / Q000494:pharmacology*; D001681:Biological Assay; D018938:Caco-2 Cells; D002374:Catalase / Q000494:pharmacology; D002478:Cells, Cultured; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000276:immunology; D019587:Dietary Supplements; D005227:Fatty Acids / Q000032:analysis; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007422:Intestines / Q000166:cytology / Q000187:drug effects; D007501:Iron / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008895:Milk, Human / Q000737:chemistry / Q000187:drug effects*; D013482:Superoxide Dismutase / Q000494:pharmacology; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D000906:Antibodies; D000975:Antioxidants; D005227:Fatty Acids; D017392:Thiobarbituric Acid Reactive Substances; D000080242:8-Hydroxy-2'-Deoxyguanosine; D007501:Iron; D002374:Catalase; D013482:Superoxide Dismutase; D003849:Deoxyguanosine; D001205:Ascorbic Acid