Cadmium exposure during pregnancy reduces birth weight and increases maternal and foetal glucocorticoids

Ronco, Ana María; Urrutia, Miguel; Montenegro, M. A.; Llanos, Miguel

doi:10.1016/j.toxlet.2009.04.008

Cited by 70 publications

(56 citation statements)

References 44 publications

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“…3 production of steroids. The decrease in body weight and ovary weight in animals exposed to Cd is consistent with previous observations [29,31]. The observed decrease in food and water consumption in Cd-treated animals might be responsible for reduced body and ovary weight.…”

Section: Discussionsupporting

confidence: 92%

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

Samuel¹,

Stanley

Princess³

et al. 2011

J. Med. Toxicol.

104

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Cadmium (Cd), an environmental pollutant, has been shown to be highly toxic to both humans and animals. Its widespread industrial use has led to its accumulation in the environment. Cd has been shown to target multiple organs following acute intoxication, causing nephrotoxicity, immunotoxicity, osteotoxicity, and reproductive toxicity. Cd can cross the placental barrier and cause a wide range of defects during fetal development. The current study was aimed to assess the effect of Cd on the female reproductive system. Female rats were exposed to Cd [50/200 ppm] from embryonic day 9 to 21 through drinking water. Serum steroid hormone concentrations, hematological parameters, antioxidant enzyme levels, and ovarian histopathology were described. Water consumption, gravid uterine/body weight decreased in both the doses of Cd-treated dams. The hematological parameters analyzed in rat pups showed a significant reduction in both doses of Cd studied, while hemoglobin showed a significant reduction in 200 ppm Cd treatment alone. MCHC levels did not show any variation in 50 ppm Cd treatment, while 200 ppm Cd treatment significantly increased. Specific activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, and serum testosterone, estradiol, and progesterone were significantly decreased. The levels of hydrogen peroxide and lipid peroxidation were increased in 50 and 200 ppm Cd-treated rats. These changes were accompanied with disrupted ovarian histoarchitecture, an extended estrous cycle, and delayed pubertal onset in Cd-treated rats. The data generated from the present study suggest that gestational Cd treatment induces ovarian toxicity and reproductive dysfunction through increased oxidative stress.

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Section: Discussionsupporting

confidence: 92%

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

Samuel¹,

Stanley

Princess³

et al. 2011

J. Med. Toxicol.

104

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“…Cd was reported to damage bone microstructures (Liu et al, 2013;Chen et al, 2011) and can negatively influence growth in newborns. Several studies have reported an inverse relationship between anthropometric measurements of the newborn and the placental or umbilical cord Cd levels (Liu et al, 2013;Llanos et al, 2009;Ronco et al, 2009). Cd exposure exerts inhibitory effects on testicular steroidogenesis (Liu et al, 2013;Pillai et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Molecular characterization and expression pattern of a novel cadmium resistance gene of tobacco

Fuzhao¹,

Zhao²

2015

Biosci. J.

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Cadmium (Cd) of tobacco is a pollutant that is extremely toxic to the health of humans. Protein plant cadmium resistance 8 gene has been characterized to increase the plant Cd resistance. In present experiment, the complete mRNA sequence of tobacco protein plant cadmium resistance 8 gene was amplified using the rapid amplification of cDNA ends methods. The full-length tobacco protein plant cadmium resistance 8 gene mRNA was 887bp containing an 555 bp open reading frame, which encodes a protein of 184 amino acids. BLAST analysis revealed that tobacco protein plant cadmium resistance 8 protein shares high homology with the protein plant cadmium resistance 8 of potato (81%), Lycopersicon esculentum (80%), Eutrema salsugineum (60%), Capsella rubella (58%) and thale cress (57%). Results also showed that tobacco protein plant cadmium resistance 8 gene has a closer genetic relationship with the protein plant cadmium resistance 8 gene of Lycopersicon esculentum. The expression profile was studied and the results indicated that tobacco protein plant cadmium resistance 8 gene was highly expressed in root, moderately expressed in stem, and hardly expressed in flower and leaf. These results established the primary foundation of utilizing tobacco protein plant cadmium resistance 8 gene to decrease the cadmium content of tobacco and benefit the health of humans in the future.

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“…Cd produces severe toxic effects in multiple tissues such as the kidney, liver, lung and bone (Järup et al, 1998;Zalups and Ahmad, 2003;Tokumoto et al, 2011). Moreover, it has been shown in animal experiments and epidemiological studies that Cd causes defective growth in the next generation (Ronco et al, 2009;Zhang et al, 2004). Accumulated Cd in neonates is also feared to affect the brain adversely (Gupta et al, 1995), although Cd transported to the neonatal brain is minimal (Ishitobi et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Microarray analysis of neonatal brain exposed to cadmium during gestation and lactation

et al. 2013

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-DNA microarray containing 30,000 genes was used to monitor the transcriptional response of the neonatal brain after cadmium (Cd) exposure. C57BL/6J pregnant mice were exposed to Cd (10 ppm) during gestation and lactation via drinking water. In a comparison between the Cd-exposed neonatal brain and control, three genes including transferrin receptor (Tfrc) were up-regulated and one gene was down-regulated.

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Cadmium exposure during pregnancy reduces birth weight and increases maternal and foetal glucocorticoids

Cited by 70 publications

References 44 publications

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

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

Molecular characterization and expression pattern of a novel cadmium resistance gene of tobacco

Microarray analysis of neonatal brain exposed to cadmium during gestation and lactation

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