@article{lichtler_klossner_smith_hoyo_cowley_2025, title={Dietary Iron Supplementation Protects Against Growth Restriction and Metabolic Dysfunction‐Associated Steatotic Liver Disease in Perinatal Cadmium‐Exposed Mice}, volume={6}, url={https://doi.org/10.1096/fba.2025-00045}, DOI={10.1096/fba.2025-00045}, abstractNote={ABSTRACT Iron (Fe)‐deficiency (ID) and Fe‐deficiency anemia (IDA) are highly prevalent conditions and are of particular concern to maternal–child health. ID and IDA are typically linked to nutritional deficiencies, but maternal exposure to heavy metals including cadmium (Cd) also leads to offspring with low levels of circulating Fe. Another comorbidity of ID and IDA is metabolic dysfunction‐associated steatotic liver disease (MASLD), a liver condition characterized by lipid accumulation and fibrosis. We have previously shown that maternal Cd exposure also leads to the development of MASLD in offspring. We hypothesized that providing Fe fortification would prevent Cd‐induced ID, which would in turn rescue offspring from growth restriction and MASLD. To test this, virgin dams were exposed to 30 ppm of cadmium chloride (CdCl 2 ) in their drinking water during the preconception, gestation, and lactation periods. Fe fortification was supplied in the form of dietary ferric citrate, which amounted to two (2×) or five times (5×) the normal dietary Fe in standard chow. Our study provides evidence that perinatal Cd exposure does not prevent absorption of supplemental Fe, and that the chosen Fe supplementation dosages are sufficient to prevent Cd‐induced growth restriction, ID, IDA, and MASLD in offspring at postnatal day 21 (PND21). Our findings suggest that Fe supplementation may be a viable therapy to prevent these developmental effects of maternal Cd exposure.}, journal={FASEB BioAdvances}, author={Lichtler, Rebecca and Klossner, Hannah and Smith, Nikia and Hoyo, Cathrine and Cowley, Michael}, year={2025}, month={Jun} }
 @article{hudson_dameris_lichtler_cowley_2025, title={The effects of developmental cadmium exposure on health and disease}, volume={18}, url={https://doi.org/10.1242/dmm.052038}, DOI={10.1242/dmm.052038}, abstractNote={Cadmium (Cd) is a naturally occurring toxic heavy metal found ubiquitously throughout the environment. Anthropogenic activities since the onset of industrialization have led to widespread environmental contamination that has substantially increased human exposure and associated health risks. As one of the top ten chemicals of major public health concern of the World Health Organization, Cd poses significant risks to human health, particularly when exposure occurs during the critical stages of development. Cd accumulates in the placenta and can be detected in cord blood and fetal and neonatal tissues, so it is crucial to understand the consequences of early-life Cd exposure and the underlying molecular mechanisms. In this Review, we provide an overview of the models currently used to study developmental Cd exposure and integrate the findings from epidemiological, animal and in vitro studies. We explore the impacts and mechanisms of early-life Cd exposure on the placenta, growth and development, and organ systems, identifying common themes across diverse model systems. Finally, we pinpoint knowledge gaps and propose key research priorities that will advance our understanding and inform mitigation strategies for reducing the developmental risks of Cd exposure.}, number={6}, journal={Disease Models & Mechanisms}, author={Hudson, Kathleen M. and Dameris, Logan and Lichtler, Rebecca and Cowley, Michael}, year={2025}, month={Jun} }