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

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)

Protective role of zinc against the toxicity induced by exposure to cadmium during gestation and lactation on testis development

“…Also, our results show that Cd was accumulated in the placenta and in fetal liver but it was not detected in the fetal testis of Cd exposed-animals. These results suggest that placenta could deter most of Cd to passing from dams to fetus [32][33][34]. Importantly, exposure to Cd in utero did not impair fetus growth since the fetal weights and the craniocaudal length at the end of gestation (GD20) of the control and Cd group were not statistically different.…”

“…The transfer of Cd through maternal milk represents the primary route of offspring exposure when rodents are exposed during both gestational and lactational periods [33,37].…”

Gestational Cadmium Exposure-Induced Ovotoxicity Delays Puberty through Oxidative Stress and Impaired Steroid Hormone Levels

“…Cd has also been shown to effect reproductive toxicity either directly targeting gonads or indirectly by interfering with the hypothalamus-pituitary-gonadal axis [12]. Pregnant and lactating female animals were reported to absorb and retain substantially more dietary Cd than do their non-pregnant counterparts [13] and Cd can be transferred to fetus [14,15]. Acute Cd exposure-induced toxicity in pregnant rats were known to cause placental necrosis and hemorrhages, with an increased rate of fetal death [16].…”

Sex‐specific effects of gestational and lactational coexposure to lead and cadmium on hepatic phase I and phase II xenobiotic/steroid‐metabolizing enzymes and antioxidant status

“…This has been well documented in both rodents [14] and humans [15]. Lactational transfer of cadmium though low is an important transfer route from dams to pups during the lactational period [16]. Inhibition of zinc-dependent enzymes [17] and metabolic changes in the fetus and postnatal hepatic tissues have also been reported, but teratogenic effects have not been frequently described [18,19] on cadmium exposure.…”