Cadmium exposure during lactation causes learning and memory-impairment in F1 generation mice: amelioration by quercetin

Halder, Sumita; Kar, Rajarshi; Galav, Vikas; Mehta, Ashish; Bhattacharya, Swapan Kumar; Mediratta, Pramod Kumari; Banerjee, Basu Dev

doi:10.3109/01480545.2015.1092042

Cited by 27 publications

(13 citation statements)

References 62 publications

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“…It is known that cadmium is embryotoxic and teratogenic ( del C Díaz et al 2014 ), which is confirmed by our results that maternal cadmium exposure (100 nM in drinking water) during pregnancy affected embryo development by reducing the birth size. During lactation, cadmium obtained through breast milk can disturb development of infants ( Cherkani-Hassani et al 2016 ; Halder et al 2016 ). However, the correlation between early-life exposure and the adult phenotypes is limited.…”

Section: Discussionmentioning

confidence: 99%

Sex-Dependent Effects of Cadmium Exposure in Early Life on Gut Microbiota and Fat Accumulation in Mice

Chen

et al. 2017

Environ Health Perspect

154

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Background:Environmental cadmium, with a high average dietary intake, is a severe public health risk. However, the long-term health implications of environmental exposure to cadmium in different life stages remain unclear.Objectives:We investigated the effects of early exposure to cadmium, at an environmentally relevant dosage, on adult metabolism and the mechanism of action.Methods:We established mouse models with low-dose cadmium (LDC) exposure in early life to examine the long-term metabolic consequences. Intestinal flora measurement by 16S rDNA sequencing, microbial ecological analyses, and fecal microbiota transplant was conducted to explore the potential underlying mechanisms.Results:Early LDC exposure (100 nM) led to fat accumulation in adult male mice. Hepatic genes profiling revealed that fatty acid and lipid metabolic processes were elevated. Gut microbiota were perturbed by LDC to cause diversity reduction and compositional alteration. Time-series studies indicated that the gut flora at early-life stages, especially at 8 weeks, were vulnerable to LDC and that an alteration during this period could contribute to the adult adiposity, even if the microbiota recovered later. The importance of intestinal bacteria in LDC-induced fat accumulation was further confirmed through microbiota transplantation and removal experiments. Moreover, the metabolic effects of LDC were observed only in male, but not female, mice.Conclusions:An environmental dose of cadmium at early stages of life causes gut microbiota alterations, accelerates hepatic lipid metabolism, and leads to life-long metabolic consequences in a sex-dependent manner. These findings provide a better understanding of the health risk of cadmium in the environment.Citation:Ba Q, Li M, Chen P, Huang C, Duan X, Lu L, Li J, Chu R, Xie D, Song H, Wu Y, Ying H, Jia X, Wang H. 2017. Sex-dependent effects of cadmium exposure in early life on gut microbiota and fat accumulation in mice. Environ Health Perspect 125:437–446; http://dx.doi.org/10.1289/EHP360

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Section: Discussionmentioning

confidence: 99%

Sex-Dependent Effects of Cadmium Exposure in Early Life on Gut Microbiota and Fat Accumulation in Mice

Chen

et al. 2017

Environ Health Perspect

154

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“…we used was determined based on a previous TBI study [31,32,33]. Many recent studies have demonstrated the importance of the therapeutic time-window after the initial TBI [19,34].…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Quercetin on Mitochondrial Biogenesis in Experimental Traumatic Brain Injury via the Nrf2 Signaling Pathway

Wang

Gao

et al. 2016

PLoS ONE

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The present investigation was carried out to elucidate a possible molecular mechanism related to the protective effect of quercetin administration against oxidative stress on various mitochondrial respiratory complex subunits with special emphasis on the role of nuclear factor erythroid 2-related factor 2 (Nrf2) in mitochondrial biogenesis. Recently, quercetin has been proved to have a protective effect against mitochondria damage after traumatic brain injury (TBI). However, its precise role and underlying mechanisms in traumatic brain injury are not yet fully understood. The aim of the present study was to investigate the effect of quercetin on the potential mechanism of these effects in a weight-drop model of TBI in male mice that were treated with quercetin or vehicle via intraperitoneal injection administrated 30 min after TBI. In this experiment, ICR mice were divided into four groups: A sham group, TBI group, TBI + vehicle group, and TBI + quercetin group. Brain samples were collected 24 h later for analysis. Quercetin treatment resulted in an upregulation of Nrf2 expression and cytochrome c, malondialdehyde (MDA) and superoxide dismutase (SOD) levels were restored by quercetin treatment. Quercetin markedly promoted the translocation of Nrf2 protein from the cytoplasm to the nucleus. These observations suggest that quercetin improves mitochondrial function in TBI models, possibly by activating the Nrf2 pathway.

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“…Data have also been published regarding QE having a protective effect against Cd-induced alterations in brain cholinergic signaling and neurotoxicity in rats [28] and regarding the ability of QE to reverse the Cd-related cognitive impairment effect in female mice that were exposed to Cd during their lactating period [29]. QE protects experimental animals from memory impairment and from anxiogenic behavior induced by Cd by preventing alterations in the activities of enzymes present in rats' cerebral cortex, hippocampus, and hypothalamus [30][31][32].…”

Section: Introductionmentioning

confidence: 99%

The In Vitro Anti-Proliferative Interaction of Flavonoid Quercetin and Toxic Metal Cadmium in the 1321N1 Human Astrocytoma Cell Line

2018

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Cadmium (Cd) is a toxic heavy metal occurring in the environment as an industrial pollutant. The systematic accumulation of Cd in the human body may lead to major health problems. Quercetin (QE) is a natural flavonoid widely distributed in plants and is a part of human diet. Many studies have demonstrated the multiple benefits of QE to humans in protecting cells of our bodies. The aim of this study was to investigate the effect of QE and Cd on the proliferation of astrocytoma 1321N1 cells. Results indicated that the simultaneous exposure of the cells to 200 µM QE and 16 μM Cd significantly reduced cell viability to 6.9 ± 1.6% with respect to vehicle-treated cells. Other experiments of QE pre-treatment followed by the exposure to Cd alone or with QE indicated significant but decreased ability of QE or Cd to reduce proliferation of the cells compared to their co-incubation. Our study suggested a synergetic anti-proliferative interaction of Cd and QE in malignantly transformed cells. This adds new information regarding the biological effects of QE.

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Cadmium exposure during lactation causes learning and memory-impairment in F1 generation mice: amelioration by quercetin

Cited by 27 publications

References 62 publications

Sex-Dependent Effects of Cadmium Exposure in Early Life on Gut Microbiota and Fat Accumulation in Mice

Sex-Dependent Effects of Cadmium Exposure in Early Life on Gut Microbiota and Fat Accumulation in Mice

Protective Effects of Quercetin on Mitochondrial Biogenesis in Experimental Traumatic Brain Injury via the Nrf2 Signaling Pathway

The In Vitro Anti-Proliferative Interaction of Flavonoid Quercetin and Toxic Metal Cadmium in the 1321N1 Human Astrocytoma Cell Line

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