Zinc as an integral component of the metabolic response to trauma.
Following injury, there is a major redistribution of zinc, as demonstrated by 65Zn tracer studies in rats receiving 20 per cent burns. This injury resulted in a rapid uptake of 65Zn into spleen, lung, wound, kidney and, particularly, liver, while the uptake of 65Zn was decreased in the brain, some muscle groups and, particularly, in bone. Simultaneously, plasma 65Zn occurred predominantly as the albumin bound fraction decreased. The total amount of tracer appearing in the wound was considerably less than that in the liver, where the induction of zinc binding protein was demonstrated in the cytosol. The synthesis of this protein may have an important regulatory role in zinc homeostasis following injury. These widespread changes in 65Zn distribution are consistent with the essential role of zinc in numerous metabolic processes and the increased metabolic activity of such tissues as the liver and the wound that follows injury. It is apparent that the liver has a central role in the early postinjury changes in zinc metabolism and that bone as well as muscle provides an available source of zinc in these circumstances.
D000818:Animals; D001842:Bone and Bones / Q000378:metabolism; D002056:Burns / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D009132:Muscles / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D014945:Wound Healing; D015032:Zinc / Q000378:metabolism / Q000502:physiology*; D015037:Zinc Radioisotopes
D002352:Carrier Proteins; D015037:Zinc Radioisotopes; D015032:Zinc