» Articles » PMID: 8277517

Cadmium-109 Metabolism in Mice. IV. Diet Versus Maternal Stores As a Source of Cadmium Transfer to Mouse Fetuses and Pups During Gestation and Lactation

Overview
Date 1993 Dec 1
PMID 8277517
Citations 5
Authors
Affiliations
Soon will be listed here.
Abstract

The transfer of 109Cd from dam to offspring during gestation and lactation was studied in uniparous mice. From 70 to 210 d of age and during the subsequent reproductive period, young adult female mice received drinking water containing tracer amounts of 109Cd (8 ppb total Cd) and nutrient-sufficient or -deficient solid diet containing stable Cd (5 ppm Cd). The nutrient quality of the deficient diet was patterned after that consumed by Japanese women who contracted itai-itai disease. To evaluate established maternal stores as a potential source of cadmium transfer to pups, some dams were switched to water with no 109Cd and diet with an environmental or control level of cadmium (0.25 ppm Cd) during the reproductive period. The resulting pups were analyzed for 109Cd at birth and at 7-d intervals throughout the lactation period. Pup 109Cd content at birth, representative of the amount transferred via the placenta during gestation, accounted for less than 1% of the total 109Cd transferred during the full reproductive period. During lactation, 109Cd levels in pups from dams with current 109Cd exposure approximately tripled with each 7-d interval; no significant differences occurred due to nutrient quality of the dams' diet. For 21-d-old pups, 98% of the 109Cd burden came from the diet of the dam, while only 2% came from her tissue stores, primarily the hepatic one. Such fractions represented a transfer per pup of about 0.01% of the oral 109Cd dose ingested by the dam during the reproductive period and about 0.05% of the 109Cd in her tissue stores. Overall, transfer per litter amounted to about 7% of the dietary 109Cd dose absorbed and retained by the dam during that interval and about 0.2% of the 109Cd from tissue stores. On lactation d 21, 90% of the total 109Cd in pups was sequestered in the gastrointestinal tract. Cadmium transfer was additionally examined in multiparous mice that began a repetitive breeding program at 70 d of age at the time of introduction to the same diet/water regimens already described. Overall, females consuming nutrient-sufficient diet experienced 5 consecutive 42-d rounds of gestation/lactation, while their deficient diet counterparts experienced 3 nonconsecutive rounds during an equivalent period. Transfer was examined during their last gestation/lactation experience. Throughout the lactation interval, 109Cd transfer to pups was about 30% increased for multiparous versus uniparous females; however, transfer again was not significantly affected by nutrient quality of the dams' diet.(ABSTRACT TRUNCATED AT 400 WORDS)

Citing Articles

The relationship between cadmium exposure and preeclampsia: a systematic review and meta-analysis.

Li C, Luo J, Yang Y, Wang Q, Zheng Y, Zhong Z Front Med (Lausanne). 2023; 10:1259680.

PMID: 38105903 PMC: 10722428. DOI: 10.3389/fmed.2023.1259680.


Early Life Environmental Exposure to Cadmium, Lead, and Arsenic and Age at Menarche: A Longitudinal Mother-Child Cohort Study in Bangladesh.

Malin Igra A, Rahman A, Johansson A, Pervin J, Svefors P, El Arifeen S Environ Health Perspect. 2023; 131(2):27003.

PMID: 36729392 PMC: 9894154. DOI: 10.1289/EHP11121.


Effects of low-dose cadmium exposure during gestation and lactation on development and reproduction in rats.

Luo X, Li L, Ma M, Li R Environ Sci Pollut Res Int. 2015; 22(14):10569-79.

PMID: 25735246 DOI: 10.1007/s11356-015-4249-5.


Influence of acute cadmium exposure on the liver proteome of a teleost fish, ayu (Plecoglossus altivelis).

Lu X, Chen J, Huang Z, Zhuang L, Peng L, Shi Y Mol Biol Rep. 2011; 39(3):2851-9.

PMID: 21667247 DOI: 10.1007/s11033-011-1044-3.


Gestational cadmium exposure-induced ovotoxicity delays puberty through oxidative stress and impaired steroid hormone levels.

Samuel J, Stanley J, Princess R, Shanthi P, Sebastian M J Med Toxicol. 2011; 7(3):195-204.

PMID: 21373971 PMC: 3550211. DOI: 10.1007/s13181-011-0143-9.