B. Elsenhans et al., SMALL-INTESTINAL ABSORPTION OF CADMIUM AND THE SIGNIFICANCE OF MUCOSAL METALLOTHIONEIN, Human & experimental toxicology, 16(8), 1997, pp. 429-434
1 Although food intake is among the most important routes of Cd exposu
re, not many details are known about the intestinal absorption mechani
sms of Cd. In this respect Cd is representative of most other nonessen
tial, merely toxic metals. 2 Based on a concept of two distinguishable
steps, intestinal absorption of Cd is characterized by high accumulat
ion within the intestinal mucosa and a low rate of diffusive transfer
into the organism. 3 After uptake into the mammalian organism, Cd is s
equestered into hepatic metallothionein (MT). It is assumed that hepat
ic Cd-MT then gradually redistributes Cd to the kidney, which is the m
ain target organ for chronic Cd toxicity. 4 When feeding low levels of
dietary CdCl2, however, Cd accumulates preferentially in the kidney a
nd to a lesser degree in the liver, a distribution pattern also found
after intravenous and peroral administration of the Cd-MT complex itse
lf. As dietary Cd induces intestinal MT, intestinal Cd-MT complexes co
uld be at least partly responsible for the renal accumulation of dieta
ry Cd. 5 For this mechanism, however, serosal release of mucosal Cd-MT
is required. In fact, in vitro findings in rats reveal a concentratio
n-dependent release of intestinal MT to the serosal side of the small
intestine. These results indicate that endogenous intestinal MT may de
liver Cd-MT to other inner organs, thus contributing to the preferenti
al renal accumulation of ingested Cd.