Send to

Choose Destination
See comment in PubMed Commons below
Life Sci. 2011 Jan 17;88(3-4):150-5. doi: 10.1016/j.lfs.2010.11.006. Epub 2010 Nov 6.

Effect of dietary selenite on development and intestinal absorption in offspring rats.

Author information

Department of Physiology and Zoology, Faculty of Pharmacy, Seville University, 41012 Seville, Spain.



The present study aims to compare selenium (Se) status in offspring rats born to selenium-deficient and selenium supplemented dams and to analyse Se's influence on intestinal parameters and the intestinal absorption of selenomethionine (Se-Met).


Male and female Wistar rats (150-200 g) were randomised in: control (C) (0.1 ppm Se), Se-deficient (SD) (0.01 ppm Se) and Se-supplemented (SS) (0.5 ppm Se) groups; and were mated to obtain their offspring. Se levels in serum, urine and faeces in offspring and in mothers' milk were measured by graphite-furnace atomic absorption spectrometry. Duodenal transport studies in offspring were performed using an in vivo perfusion of different Se-Met concentrations (2, 5, 10, 25, 75 and 150 μM).


A Se-deficient diet provoked a decrease in the offspring's body weight and intestinal parameters, while the supplemented diet increased these values. Serum Se levels were similar between Se-deficient and control offspring because the urinary excretion of Se was smaller to compensate for Se homeostasis. Intestinal Se-Met absorption obeys the Michaelis-Menten equation with lower apparent constant (K(m)) and maximal velocity (V(max)) in the SD group. However, the C and SS groups presented similar K(m) and different V(max). The V(max) showed greater values in the following order of rank: SS>C>SD groups.


Selenium intake deficiencies in offspring lead to the development of compensatory mechanisms in order to normalise serum selenium levels. These mechanisms, however, do not permit normal body development; nor do they regulate intestinal parameters and Se-Met transport.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center