Editor’s Highlight: Exposure to CrVI during Early Pregnancy Increases Oxidative Stress and Disrupts the Expression of Antioxidant Proteins in Placental Compartments

Banu, Sakhila K.; Stanley, Jone A.; Sivakumar, Kirthiram K.; Taylor, Robert J.; Arosh, Joe A.; Burghardt, Robert C.

doi:10.1093/toxsci/kfw231

Cited by 9 publications

(5 citation statements)

References 55 publications

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“…Shown here, the 48 h exposure of human trophoblasts to E in vitro and in utero in rats resulted in a reduction of PCNA and CYCLIN-D1 expression (Figure 6 and Figure 7). Abridged PCNA and CYCLIN-D1 levels have been previously shown to impair the placental development in conditions that are underscored by oxidative stress akin to E [64,65]. While E-induced diminution of proliferation-associated proteins such as PCNA and CYCLIN-D1 which closely correlated with a reduction in the proliferative capacity in vitro, this was not reflected in the in utero E exposed rats with the unchanged placental and body weights (Figure 2).…”

Section: Discussionmentioning

confidence: 90%

Ethanol Impairs NRF2/Antioxidant and Growth Signaling in the Intact Placenta In Vivo and in Human Trophoblasts

et al. 2019

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NRF2 is a redox-sensitive transcription factor that depending on the duration or magnitude of the stress, either translocates to the nucleus (beneficial) or is degraded in the cytosol (harmful). However, the role of NRF2-based mechanism(s) under ethanol (E)-induced developmental toxicity in the placental context remains unknown. Here, we used a rat prenatal model of maternal alcohol stress consisting of intermittent ethanol vapor (IEV) daily from GD11 to GD20 with a 6 h ON/18 h OFF in a vapor chamber and in vitro placental model consisting of HTR-8 trophoblasts exposed to 86 mM of E for either 24 h or 48 h. The role of NRF2 was evaluated through the NRF2-transactivation reporter assay, qRT-PCR, and Western blotting for NRF2 and cell growth-promoting protein, and cell proliferation assay. In utero and in vitro E decreased the nuclear NRF2 content and diminished its transactivation ability along with dysregulation of the proliferation indices, PCNA, CYCLIN-D1, and p21. This was associated with a ~50% reduction in cell proliferation in vitro in trophoblasts. Interestingly, this was found to be partially rescued by ectopic Nrf2 overexpression. These results indicate that ethanol-induced dysregulation of NRF2 coordinately regulates PCNA/CYCLIN-D1/p21 involving growth network, at least partially to set a stage for placental perturbations.

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Section: Discussionmentioning

confidence: 90%

Ethanol Impairs NRF2/Antioxidant and Growth Signaling in the Intact Placenta In Vivo and in Human Trophoblasts

et al. 2019

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“…These findings emphasize the crucial role of the placental barrier in protecting the developing fetus from genotoxic agents. Additional studies, such as those conducted by Banu et al (2017, 2018), demonstrated accumulation of Cr(VI) in the placenta and consequent adverse effects on placental functions, including disruption of trophoblast cells, increased oxidative stress, and changes in antioxidant levels. Understanding the role of the placenta in the distribution of genotoxic agents is essential for assessing risks and implementing preventive measures during embryonic and fetal development.…”

Section: Discussionmentioning

confidence: 94%

“…These findings emphasize the crucial role of the placental barrier in protecting the developing fetus from genotoxic agents. Additional studies, such as those conducted by Banu et al (2017Banu et al ( , 2018 a prolonged genotoxic impact on the hematopoietic system. The enhanced susceptibility of the developing hematopoietic system to genotoxic substances has significant implications for various disorders, including neurodegenerative diseases, blood disorders, skin disorders, and cancers (Udroiu & Sgura, 2016).…”

Section: Effects During Pregnancymentioning

confidence: 99%

A comparative study on chromium‐induced micronuclei assessment in the peripheral blood of Hsd:ICR mice

García‐Rodríguez,

Hernández‐Cortés,

Montaño‐Rodríguez

et al. 2023

J of Applied Toxicology

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This study investigated the genotoxic effects of chromium (Cr) in Hsd:ICR mice, considering factors such as oxidative state, apoptosis, exposure pathway, duration, pregnancy, and transplacental exposure. Genotoxicity was assessed using the erythrocytes' micronucleus (MN) assay, while apoptosis was evaluated in nucleated blood cells. The results showed that Cr(III) (CrK(SO4)2 and CrCl3) did not induce any marked genotoxic damage. However, Cr(VI) (CrO3, K2Cr2O7, Na2Cr2O7, and K2CrO4) produced varying degrees of genotoxicity, with CrO3 being the most potent. MN frequencies increased following 24‐h exposure, with a greater effect in male mice. Administering 20 mg/kg of CrO3 via gavage did not lead to significant effects compared to intraperitoneal administration. Short‐term oral treatment with a daily dose of 8.5 mg/kg for 49 days elevated MN levels only on day 14 after treatment. Pregnant female mice exposed to CrO3 on day 15 of pregnancy exhibited reduced genotoxic effects compared to nonpregnant animals. However, significant increases in MN levels were found in their fetuses starting 48 h after exposure. In summary, data indicate the potential genotoxic effects of Cr, with Cr(VI) forms inducing higher genotoxicity than Cr(III). These findings indicate that gender, exposure route, and pregnancy status might influence genotoxic responses to Cr.

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“…In animal studies, chromium VI induced developmental toxicity of placenta through downregulating cell survival proteins and increasing cell death by spatiotemporal modulation of apoptotic signaling 54 . The imbalance between ROS and AOXs induced by chromium VI may be one of the mechanisms which potentially affect placental growth and fetal development and thus increased risk of preterm birth 55 . In the stratified analysis, we found that the associations may vary by infant gender in our study, as the significant association between maternal urinary chromium levels and risk of delivering preterm birth was stronger in male infants than in female.…”

Section: Discussionmentioning

confidence: 99%

Prenatal chromium exposure and risk of preterm birth: a cohort study in Hubei, China

Pan

Xia

et al. 2017

Sci Rep

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Few studies have investigated the association of environmental chromium exposure and preterm birth in general population. This study was designed to investigate whether maternal chromium exposure during pregnancy is associated with reduced gestational age or risk of preterm birth using the data from Healthy Baby Cohort study conducted in Hubei, China between 2012 and 2014 (n = 7290). Chromium concentrations in maternal urine samples collected at delivery were measured with inductively coupled plasma mass spectrometry. Tertiles of chromium concentrations was negatively associated with gestational age in multivariable linear regression analyses [β (95% CI): low = reference; middle = −0.67 days (−1.14, −0.20); high = −2.30 days (−2.93, −1.67); p trend <0.01]. Logistic regression analyses also indicated that higher maternal chromium [adjusted odds ratio (OR) (95% CI): 1.55(0.99, 2.42) for the medium tertile; 1.89(1.13, 3.18) for the highest tertile; p trend <0.01] was associated with increased risk of preterm birth. The associations appeared to be more pronounced in male infants (adjusted OR (95% CI): 2.54 (1.29, 4.95) for the medium tertile; 2.92 (1.37, 6.19) for the highest tertile; p trend <0.01). Our findings suggest maternal exposure to higher chromium levels during pregnancy may potentially increase the risk of delivering preterm infants, particularly for male infants.

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Editor’s Highlight: Exposure to CrVI during Early Pregnancy Increases Oxidative Stress and Disrupts the Expression of Antioxidant Proteins in Placental Compartments

Cited by 9 publications

References 55 publications

Ethanol Impairs NRF2/Antioxidant and Growth Signaling in the Intact Placenta In Vivo and in Human Trophoblasts

Ethanol Impairs NRF2/Antioxidant and Growth Signaling in the Intact Placenta In Vivo and in Human Trophoblasts

A comparative study on chromium‐induced micronuclei assessment in the peripheral blood of Hsd:ICR mice

Prenatal chromium exposure and risk of preterm birth: a cohort study in Hubei, China

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