...the protein product of IGFBP1 also was lower than controls in zinc-deficient rats
Brain Res. 2005 Jun 28;1048(1-2):228-34.
Morphological alterations produced by zinc deficiency in rat sciatic nerve: a histological, electron microscopic, and stereological study.
Unal B, Tan H, Orbak Z, Kiki I, Bilici M, Bilici N, Aslan H, Kaplan S.
Zinc (Zn) is an essential trace element for humans and animals. It is required for normal growth, gene expression, wound healing, protein metabolism, immune function, and membrane integrity. In this study, unbiased stereological methods have been used to quantify the effects of Zn deficiency on the sectioned surface area and the number of myelinated axons in the sciatic nerve of rats. Animals were fed a Zn-deficient or Zn-sufficient diet for a period of 4 weeks. At the end of this time, the samples of sciatic nerves were removed from the animals, processed for electron microscopy and embedded in resin. The Zn-deficient group of rats was found to have a lower body weight compared to rats in the control group (P < 0.05). The sectioned surface area of nerve cross-section and myelinated axon number in Zn-deficient rats decreased by 20% and 29%, respectively, compared to the control group. A significant correlation between sectioned surface area and myelinated axon number was also determined. Morphological findings were as follows: on light microscopy, it was determined that certain abnormalities occur specifically in the experimental group, such as collapsed nerve fascicles, irregular profiles of and degeneration in myelin sheaths, and on electron microscopy, extensive myelin damage was seen in Zn-deficient groups compared with control groups. This study suggests that peripheral nerves require Zn for development and preservation of their structure.
Users browsing this forum: harry1