Association between exposure to arsenic, nickel, cadmium, selenium, and zinc and fasting blood glucose levels

Li, Zhaoyang; Xu, Yajuan; Huang, Zhijun; Wei, Yonggang; Hou, Jian; Long, Tengfei; Wang, Fei; Hu, Hua; Duan, Yanying; Guo, Huan; Zhang, Xiaomin; Chen, Xiang; Yuan, Hong; Wu, Tangchun; Shen, Min; He, Meian

doi:10.1016/j.envpol.2019.113325

Cited by 58 publications

(31 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Silver nanoparticles (AgNP) induces ER stress and autophagy through the Ca 2+ / CAMKK / AMPK / mTOR pathway. The specific mechanism is that CAMKK and AMPK are activated by the increase of Ca 2+ levels in the cytoplasm after being stimulated by AgNP, which leads to the downregulation of mTOR and the upregulation of Beclin1 , eventually activating autophagy ( Li et al., 2019a , Li et al., 2019b ). In our experiment, Se deficiency also caused the accumulation of autophagy in the swine small intestine by increasing the expression of CAMKK-β and AMPK in the Ca 2+ / CAMKK-β / AMPK / mTOR pathway and decreasing the expression of mTOR .…”

Section: Discussionmentioning

confidence: 99%

“…In our experiment, the contents of B, V, and Cu were reduced in Se-deficiency, which could increase the risk of dementia, autism, and depression ( Janka, 2019 ). Decreased levels of Ni and Al affect fasting blood glucose ( Li et al., 2019a , Li et al., 2019b ). Increased Ca content can exacerbate the risk of diabetes, even accumulation of Ca 2+ in mitochondria and promote apoptosis ( Kahya et al., 2017 ).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

et al. 2021

View full text Add to dashboard Cite

Selenium (Se) deficiency can seriously affect the small intestine of swine, and cause diarrhea in swine. However, the specific mechanism of Se deficiency-induced swine diarrhea has rarely been reported. Here, to explore the damage of Se deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal Se deficiency were established. Twenty-four pure line castrated male Yorkshire pigs (45 d old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into 2 equal groups and fed Se-deficient diet (0.007 mg Se/kg) as the Se-deficiency group, or fed Se-adequate diet (0.3 mg Se/kg) as the control group for 16 weeks. The intestinal porcine enterocyte cell line (IPEC-J2) was divided into 2 groups, and cultured by Se-deficient medium as the Se-deficient group, or cultured by normal medium as the control group. Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. Autophagy staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. According to the reactive oxygen species (ROS) staining results, the percentage of ROS in the Se-deficiency group was higher than that in the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy-calcium-related genes including Beclin 1 , microtubule-associated proteins 1A ( LC3-1 ), microtubule-associated proteins 1B ( LC3-2 ), autophagy-related protein 5 ( ATG5 ), autophagy-related protein 12 ( ATG12 ), autophagy-related protein 16 ( ATG16 ), mammalian target of rapamycin ( mTOR ), calmodulin-dependent protein kinase kinase β ( CAMKK-β ), adenosine 5′-monophosphate-activated protein kinase ( AMPK ), sarco(endo)plasmic reticulum Ca 2+ -ATPase ( SERCA ), and calpain in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro ( P < 0.05). Altogether, our results indicated that Se deficiency could destroy the calcium homeostasis of the swine small intestine to trigger cell autophagy and oxidative stress, which was helpful to explain the mechanism of Se deficiency-induced diarrhea in swine.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

et al. 2021

View full text Add to dashboard Cite

show abstract

“…In this experiment, the contents of B, V and Cu were reduced by selenium de ciency, which could increase the risk of dementia, autism and depression [66]. Decreased levels of Ni and Al affect fasting blood glucose [67]. Increased Ca content can exacerbate the risk of diabetes, and even accumulation of Ca 2+ in mitochondria will promote apoptosis [68].…”

Section: Discussionmentioning

confidence: 99%

Calcium Overload and Ros Accumulation Induced by Selenium Deficiency Promote Autophagy in Swine Intestine

Zheng¹,

Guan²,

Yang³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background:Selenium deficiency can seriously affect the intestinal status of swine, and cause diarrhea in swine. However, the specific mechanism of selenium intestinal injury caused by selenium deficiency is rarely reported.Methods:Here, to explore the damage of selenium deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal selenium deficiency were established. The intestinal model of swine intestine was established by feeding different selenium concentrations. Besides, selenium-deficient medium and normal medium were used to culture IPEC-J2 cells to establish in vitro models. Morphological observation and cell staining were used to determine the way of intestinal injury, and gene expression was quantitatively detected by qPCR and WB.Results:Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. MDC staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. Also, according to the ROS test results, the percentage of ROS in the Se-deficiency group is higher than the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy and calcium-related genes (Beclin1, LC3-1, LC3-2, ATG5, ATG12, ATG16, mTOR, CAMKK-β, AMPK, SERCA, calpain) in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro. Under the influence of selenium deficiency, the mRNA expression level of selenoproteins decreased significantly, and the steady-state content of some elements was also destroyed. Conclusion:Altogether, our results indicated that selenium deficiency could destroy the calcium homeostasis and antioxidant homeostasis of swine intestine to trigger cell autophagy. Moreover, selenium deficiency reduces the overall expression of selenoproteins and affects the content of elements in the intestine.

show abstract

“…The differences may be due to that these previous studies mainly obtained the independent relationship between TAs or iAs with As methylation indices by linear regression analysis, while we not only obtained the nonlinear relationship between TAs and iAs with those indices and analyzed the possible combined effects by BKMR analyses. Besides, this method allowed for a more accurate correlation between one variable and an outcome while controlling an other variable that we also wanted to study (Li and Xu et al 2019;Wang and Gao et al 2020). Speci cally, when we analyzed the relationship between TAs and methylation capacity, iAs was set at a speci c level; otherwise, TAs was set at a speci c level.…”

Section: Tas and Ias Levelsmentioning

confidence: 99%

Influencing Trend and Extent of Combined Exposure Levels of Total Arsenic and Inorganic Arsenic on Arsenic Methylation Capacity Among University Students: Findings from Bayesian Analysis Using Kernel Machine Regression

Jiang

Zhang

et al. 2021

Preprint

View full text Add to dashboard Cite

The arsenic (As) methylation capacity is an important determinant of the susceptibility to arsenic-related diseases. Total As (TAs) or inorganic As (iAs) was reported to associate with As methylation capacity individually, however, influencing trend and extent of their combined exposure levels on methylation capacity remains poorly understood. We measured urinary concentrations of iAs, monomethylarsonic (MMA), and dimethylarsinic (DMA) acids using HPLC-HG-AFS, and calculated the primary (PMI: (MMA+DMA)/TAs) and secondary (SMI: DMA/(MMA+DMA)) methylation capacity indexes in 209 university students in Hefei, China, a non-As endemic area. Subjects were given with a standardized questionnaire to inquire their sociodemographic characteristics. Bayesian kernal machine regression (BKMR) analysis was used to estimate the association of lnTAs and lniAs levels with methylation indices (ln%MMA, ln%DMA, lnPMI, lnSMI). The median concentration of iAs, MMA and DMA was 1.22, 0.92 and 12.17 μg/L, respectively; the proportions of iAs, MMA and DMA were 8.76%, 6.13% and 84.84%, respectively. Females had higher %DMA and lower %MMA, while males had lower %DMA and higher %MMA. The combined levels of lnTAs and lniAs showed monotonic decrease in change of ln%DMA and lnSMI other than ln%MMA, additionally, change in ln%PMI was decreased only when levels of lnTAs and lniAs were larger than their 60th percentiles compared to they were at 50th percentile. With regard to single exposure level, the lnTAs showed positive correlation with ln%DMA, lnPMI, lnSMI when lniAs was set at a specific level; while lniAs showed negative correlation with ln%DMA, lnPMI, lnSMI when lnTAs was set at a specific level; and all the dose-response relationships were nonlinear. Our results suggested that combined levels of TAs and iAs played an important role in reducing As methylation capacity, expecially iAs; and the reduction only occured when TAs and iAs were up to a certain combined level.

show abstract

Association between exposure to arsenic, nickel, cadmium, selenium, and zinc and fasting blood glucose levels

Cited by 58 publications

References 65 publications

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

Calcium Overload and Ros Accumulation Induced by Selenium Deficiency Promote Autophagy in Swine Intestine

Influencing Trend and Extent of Combined Exposure Levels of Total Arsenic and Inorganic Arsenic on Arsenic Methylation Capacity Among University Students: Findings from Bayesian Analysis Using Kernel Machine Regression

Contact Info

Product

Resources

About