title: Metallothionein is induced and trace element balance changed in target organs of a common viral infection.
abstract: In experimental studies on the common human coxsackievirus B type 3 (CB3) infection, administered cadmium (Cd) is known to accumulate in the liver and kidneys. CB3 adapted to Balb/c mice was used to study whether infection affects the Cd-binding protein, metallothionein (MT) and if this alters the normal physiological trace element balance in the liver, kidney, spleen and brain. On day 3 of infection, degradation of liver proteins (44%, P<0.01) occurred, whereas in the spleen, protein increased (63%, P<0.05). The infection increased MT five-fold (P<0.01) in liver and kidneys, and in spleen by 34% (P<0.05). A redistribution of Cd and copper (Cu) from the liver to the kidney was associated with this increase in MT, resulting in an increased (P<0.01) kidney/liver ratio for both elements. The infection increased the zinc (Zn) concentration more in the kidney than in the liver, but the kidney/liver ratio was not significantly affected. Results show that MT is increased in several organs during the early phase of infection and is associated with redistribution of both essential and non-essential trace elements. This may be a normal response in common infections that could adversely influence the pathogenesis when the host is concomitantly exposed to potentially toxic trace elements, even at levels in the physiological range.
authors.affiliation: Toxicology Division, Swedish National Food Administration, P.O. Box 622, Uppsala S-751 26, Sweden. nils-gunnar.ilback@slv.se
authors.forename: Nils-Gunnar
authors.initials: NG
authors.lastname: Ilbäck
authors.forename: Anders W
authors.initials: AW
authors.lastname: Glynn
authors.forename: Lotta
authors.initials: L
authors.lastname: Wikberg
authors.forename: Elvy
authors.initials: E
authors.lastname: Netzel
authors.forename: Ulf
authors.initials: U
authors.lastname: Lindh
mesh_terms: D000210:Acute-Phase Reaction / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D002104:Cadmium / Q000378:metabolism; D003300:Copper / Q000378:metabolism; D004195:Disease Models, Animal; D029822:Enterovirus B, Human / Q000472:pathogenicity / Q000502:physiology; D004769:Enterovirus Infections / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D005260:Female; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008668:Metallothionein / Q000096:biosynthesis*; D051379:Mice; D008807:Mice, Inbred BALB C; D009929:Organ Size; D011506:Proteins / Q000378:metabolism; D013154:Spleen / Q000378:metabolism / Q000473:pathology; D014131:Trace Elements / Q000378:metabolism*; D015032:Zinc / Q000378:metabolism
chemical_list: D011506:Proteins; D014131:Trace Elements; D002104:Cadmium; D003300:Copper; D008668:Metallothionein; D015032:Zinc