Toxicogenomic study in rat thymus of F1 generation offspring following maternal exposure to silver ion (original) (raw)
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Environmental Toxicology and Pharmacology
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Folia Veterinaria, 2019
The aim of this investigation was to evaluate the effects of the exposure to low doses of lead, mercury and cadmium dissolved in drinking water (200× above maximal permissible dosage) on the reproductive potency of 200 Wistar rats (100 males and 100 females of F1 generation) and their progeny. Ten groups of rats were formed according to their exposure to heavy metals, including one control group without exposure. The females gave births between weeks 13 and 78 of the experiments. Reproduction parameters, such as number of litters, total number of newborns, number of newborns per litter, and number of weanlings were assessed weekly. The results demonstrated that the number of litters and newborns were higher after exposure to mercury and lower after exposure to lead. The number of weanlings and their share from newborns were the highest after exposure to cadmium and the lowest after exposure to mercury. A sex-specific effect of metals was related to the reproductive success.
Birth Defects Research, 2019
Background: Silver nanoparticles (SNPs) are being increasingly used in medical and industrial products. The aim of the present study was to evaluate the toxic effect of maternal exposure to SNP (1 mg/kg/day, 70 nm) on fetal development during the first and second weeks of pregnancy. Methods: Twenty-four pregnant mice were divided into four groups. SNP was administered by oral gavage on gestational days (GD) 1-7, GD8-14, or GD1-14. Phosphate buffered saline was administered by oral gavage to a control group. On GD15, the uteri were excised, and fetal bodies and placentas were weighed. Head and placental circumferences and fetal crown-rump length were measured, and fetuses were evaluated for external malformation. TUNEL assay was performed to assess apoptosis in the fetal midbrain. Hematoxylin-eosin staining was carried out to determine changes in fetal histomorphology. Fetal liver cells were used for karyotype analysis. Results: Significant decreases in fetal body weight, and crown-rump length were observed in SNP-treated groups. Exencephaly, small head, scoliosis, lordosis, short thorax and trunk, also fused digits were detected in SNPs-treated groups. Fibrosis, necrosis, and apoptotic cells in fetal midbrains increased significantly in the GD8-14 and GD1-14 groups compared to the control group. Chromosomal features were not different in fetuses between groups. Conclusions: Exposure to 1 mg/kg/day SNP during pregnancy in mice adversely affected on fetal development. The results do suggest a potential risk for humans that needs to be followed up with more definitive investigations.
Reproductive Toxicology, 2007
Tributyltin (TBT) is an environmental contaminant commonly used in anti-fouling agents for boats, as well as a by-product from several industrial processes. It has been shown to accumulate in organisms living in areas with heavy maritime traffic thereby entering the food chain. Here, we determined the consequences of in utero exposure to TBT on the developing fetal gonads in the Sprague-Dawley rat. Timed pregnant rats were gavaged either with vehicle or TBT (0.25, 2.5, 10 or 20 mg/kg) from days 0 to 19 or 8 to 19 of gestation. On gestational day 20, dams were sacrificed; fetal testes and ovaries were processed for light (LM) or electron microscopic (EM) evaluation and RNA was prepared for gene expression profiling. At the highest doses of TBT the number of Sertoli cells and gonocytes was reduced, there were large intracellular spaces between Sertoli cells and gonocytes and there was an increased abundance of lipid droplets in the Sertoli cells; EM studies revealed abnormally dilated endoplasmic reticulum in Sertoli cells and gonocytes. In the intertubular region between adjacent interstitial cells, immunostaining for the gap junctional protein connexin 43 was strong in controls, whereas it was reduced or completely absent in treated rats. In the ovaries, TBT (20 mg/kg, days 0-19; 10 mg/kg, days 8-19) reduced the number of germ cells by 44% and 46%, respectively. On examining gene expression profiles in the testis, 40 genes out of 1176 tested were upregulated more than two-fold over control. While no genes were upregulated in the TBT exposed fetal ovary, eight genes were downregulated. In conclusion, in utero exposure to TBT resulted in gender-specific alterations in gonadal development and gene expression profiles suggesting that there may be different adaptive changes to toxicity in developing male and female rats.
Human exposure to arsenic in countries known for heavy arsenic load, where ground water arsenic level exceeds the WHO limit, can be detrimental for developing gonads. Developmental and reproductive toxicity of arsenic in rodents after in utero exposure is although known but information on the toxic effects of arsenic on postnatal gonadal development is scant. This aspect was the focus of the present investigation. Postnatal day 25 prepubertal male mice were challenged with sub-chronic and chronic (up to PND 53 & PND 114 respectively) oral exposure (drinking water) to low and high doses (0.01, 5, and 10 mg.L-1) of sodium arsenite. Data were compared statistically at P<0.05. Sub-chronic exposure to high arsenic doses led to significant increase in the production of reactive oxygen species and lipid peroxidation, while simultaneous significant reduction occurred in the activity of antioxidant enzymes catalase, superoxide dismutase and peroxidase, hormone concentrations (folliclestimulating hormone, luteinizing hormone, testosterone) and sperm parameters. Testicular cell damage and sperm DNA damage, as revealed by comet assay, were evident at 10 mg.L-1 arsenic dose. Chronic exposure further aggravated the adverse effects. Severe testicular oxidative stress, reduction in hormones and pronounced histological alterations in testis and epididymis, and sperm parameters together with excessive sperm DNA damage were noticeable even at the lowest test dose of 0.01 mg.L-1. The study concludes that arsenic exposure considerably affects the prepubertal gonad, may cause irreversible damage to the developing reproductive system of males and that minute quantity of arsenic in drinking water can be a serious health hazard.
2012
3 Abstract: Sodium arsenite was orally administered to mice during pregnancy and lactation at a dose level of 0.4 ppm and body weights and organ weights with special focus to reproductive organs in next generation adult male mice were analyzed. The body weight and weight gain of control and experimental pups did not differ significantly. However, the weights of testes, prostate and seminal vesicle decreased in experimental mice when compared with controls. Histology of testes indicated decrease in primary and secondary spermatocytes and spermatids in experimental mice when compared with control. These results indicated that exposure to arsenic during early stages of development suppresses the development of male reproductive organs in adults. Thus, it was conclude that the potential of reproduction is programmed, to some extent, in the early stages of development and hence any toxic insult during embryonic development and lactation suppresses male reproductive potential in adulthood.
Effect of Transplacental and Lactational Exposure to Arsenic on Male Reproduction in Mice
… of Reproduction and …, 2011
Sodium arsenite was orally administered to mice during pregnancy and lactation at a dose level of 0.4 ppm and spermatogenesis of next generation in adult male mice was analyzed. A significant depletion in sperm count, sperm motility, sperm viability and HOS-coiling was observed in mice exposed to arsenic during early stages of development with an increase in sperm abnormalities. These results indicated that exposure to arsenic during early stages of development suppresses the male reproduction in adults. Thus, it was concluded that the potential of reproduction is programmed, to some extent, in the early stages of development and hence any toxic insult during embryonic development and lactation suppresses male reproductive potential in adulthood.
Biochimica et Biophysica Acta (BBA) - Biomembranes, 2007
Waterborne free silver can cause osmo-and ionoregulatory disturbances in freshwater organisms. The effects of a short-term exposure to extracellular Ag + ions on membrane currents were investigated in voltage-clamped defolliculated Xenopus oocytes. At a holding potential of −60 mV, ionic silver (1 μM Ag + ) increased inward currents (=I Ag ) from −8 ± 2 nA to − 665 ± 41 nA (n = 74; N = 27). I Ag activated within 2 min of silver exposure and then rose impetuously. This current was largely reversible by washout and repeatable. I Ag reversed around −30 mV and rectified slightly at more positive potentials. Na + -free bath conditions reduced the silver-induced current to a smaller but sustained current. The response to silver was abolished by the Cl − channel blockers DIDS and SITS, whereas niflumic acid strongly potentiated I Ag . Intraoocyte injection of AgNO 3 to about 1 mM [Ag] i strongly potentiated I Ag . Extracellular application of either dithiothreitol (DTT), a compound known to reduce disulfide bridges, or L-cysteine abolished Ag + -activated increase of membrane current. In contrast, n-ethylmaleimide (NEM) which oxidizes SHgroups potentiated I Ag . Hypoosmotic bath solution significantly increased I Ag whereas hyperosmolar conditions attenuated I Ag . The activation of I Ag was largely preserved after chelation of cytosolic Ca 2+ ions with BAPTA/AM. Taken together, these data suggest that Xenopus oocytes are sensitive to short-term exposure to waterborne Ag + ions and that the elicited membrane currents result from extra-and intracellular action of Ag + ions on peptide moieties at the oocyte membrane but may also affect conductances after internalization.