作者: Helena Öhrvik
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摘要: Cadmium is a ubiquitous toxic metal known to cause several adverse health effects in humans. Newborns have an increased gastrointestinal absorption of cadmium compared adults and seem be more sensitive toxicity. The wellestablished association between uptake dietary low iron status has not been investigated newborns. aim this thesis was study during the neonatal period, focusing on intracellular transport pathways interactions with calcium iron. Cadmium-induced lactating mammary gland were mice murine epithelial HC11 cells. reduced total levels, expression secretory pathway calcium-ATPase (SPCA) β-casein gene both vivo vitro. An involution-like remodeling tissue, including fat content, observed following exposure. results indicate that disturbs function by reducing calcium, SPCA levels secreting impact across intestine suckling piglets human immature intestinal Caco-2 High did restrict piglets; instead detected. Similar obtained Gene protein expressions localizations transporters DMT1, DMT1-IRE FPN1 affected status, indicating mechanism regulating age-dependent. multidrug resistance associated 1 (MRP1) cells treated correlated In conclusion, exposure may decrease milk potential negative developmental neonate. Furthermore, supplementation does restrict, but rather increases newborns, which should considered risk assessment cadmium.