Determination of arsenicals in mouse tissues after simulated exposure to arsenic from rice for sixteen weeks and the effects on histopathological features

Wang, Jiating; Zhang, Guiwei; Lin, Zeheng; Luo, Yu; Fang, Heng; Yang, Linjie; Xie, Jinlu; Guo, Lianxian

doi:10.1016/j.ecoenv.2020.110742

Cited by 23 publications

(8 citation statements)

References 52 publications

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“…One gut selected randomly from each glass tank was regarded as one sample ( n = 6) and used for DNA extraction. The microbiota was characterized by 16S rRNA gene sequencing at the V4–V5 hypervariable region and analyzed as described previously. , Raw data sequences of bacteria were deposited in the NCBI Sequence Read Archive under the Bioproject ID PRJNA905175 and PRJNA970036 (). After acquiring the normalized operational taxonomic units (OTUs), microbial analyses (Supporting Information Note 1) were conducted referring to our previous study …”

Section: Methodsmentioning

confidence: 99%

“…Arsenic determination was carried out following our previous method. 40 Briefly, the C tAs values of skin and muscle samples were accurately determined by ICP−MS (Agilent 7800, Santa Clara, CA, USA). Five common As species of muscle samples, including iAs V , iAs III , dimethylarsinate (DMA), monomethylarsonate (MMA), and arsenobetaine (AsB) were separated and measured by high-performance liquid chromatography coupled to ICP-MS (HPLC−ICP-MS, Agilent 1260, Palo Alto, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Approximately 100 mg of tissue or 100 μL of water sample was generated as one sample separately ( n = 6). Arsenic determination was carried out following our previous method . Briefly, the C tAs values of skin and muscle samples were accurately determined by ICP–MS (Agilent 7800, Santa Clara, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

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Effects of Intestinal Microbiota on the Biological Transformation of Arsenic in Zebrafish: Contribution and Mechanism

Zhong,

Zhang,

Huang

et al. 2024

Environ. Sci. Technol.

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Both the gut microbiome and their host participate in arsenic (As) biotransformation, while their exact roles and mechanisms in vivo remain unclear and unquantified. In this study, as3mt −/− zebrafish were treated with tetracycline (TET, 100 mg/ L) and arsenite (iAs III ) exposure for 30 days and treated with probiotic Lactobacillus rhamnosus GG (LGG, 1 × 10 8 cfu/g) and iAs III exposure for 15 days, respectively. Structural equation modeling analysis revealed that the contribution rates of the intestinal microbiome to the total arsenic (tAs) and inorganic As (iAs) metabolism approached 44.0 and 18.4%, respectively. Compared with wild-type, in as3mt −/− zebrafish, microbial richness and structure were more significantly correlated with tAs and iAs, and more differential microbes and microbial metabolic pathways significantly correlated with arsenic metabolites (P < 0.05). LGG supplement influenced the microbial communities, significantly up-regulated the expressions of genes related to As biotransformation (gss and gst) in the liver, down-regulated the expressions of oxidative stress genes (sod1, sod2, and cat) in the intestine, and increased arsenobetaine concentration (P < 0.05). Therefore, gut microbiome promotes As transformation and relieves As accumulation, playing more active roles under iAs stress when the host lacks key arsenic detoxification enzymes. LGG can promote As biotransformation and relieve oxidative stress under As exposure.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Effects of Intestinal Microbiota on the Biological Transformation of Arsenic in Zebrafish: Contribution and Mechanism

Zhong,

Zhang,

Huang

et al. 2024

Environ. Sci. Technol.

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“…A certified reference material of fish tissue (DORM-4; (Last accessed on 19 May 2022) was included to monitor sample recovery for the digestion protocol. Total arsenic levels and arsenic species were measured as described [ 33 , 34 ], at the Arizona Laboratory for Emerging Contaminants (ALEC) of the University of Arizona, using an Agilent 8900 inductively coupled plasma-mass spectrometer (ICP-MS) (Santa Clara, CA, USA). LC separation was performed on a Hamilton PRP-X100 column and guard cartridge (Hamilton Company, Reno, NV, USA), with a gradient of ammonium carbonate mobile phase (10 to 50 mM) at pH 8.6.…”

Section: Methodsmentioning

confidence: 99%

“…LC separation was performed on a Hamilton PRP-X100 column and guard cartridge (Hamilton Company, Reno, NV, USA), with a gradient of ammonium carbonate mobile phase (10 to 50 mM) at pH 8.6. The solution analyzed for arsenic species was also used to measure the total arsenic using ICP-MS, as described [ 33 , 34 ].…”

Section: Methodsmentioning

confidence: 99%

Differential Effects of Arsenic in Drinking Water on Mouse Hepatic and Intestinal Heme Oxygenase-1 Expression

Fan

et al. 2022

Antioxidants

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Arsenic exposure has been associated with the risks of various diseases, including cancers and metabolic diseases. The aim of this study was to examine the effects of arsenic exposure via drinking water on the expression of heme oxygenase-1 (HO-1), a major responsive gene to arsenic-induced oxidative stress, in mouse intestinal epithelial cells which is the first site of exposure for ingested arsenic, and the liver, a known target of arsenic toxicity. The expression of HO-1 was determined at mRNA, protein, or enzymic activity levels in mice exposed to sodium arsenite through drinking water, at various doses (0, 2.5, 10, 25, 100 ppm), and for various time periods (1, 3, 7, or 28 days). HO-1 was significantly induced in the intestine, but not liver, at arsenic doses of 25 ppm or lower. The intestinal HO-1 induction was seen in both males and females, plateaued within 1–3 days of exposure, and was accompanied by increases in microsomal HO activity. In mice exposed to 25-ppm of arsenite for 7 days, total arsenic and As(III) levels in intestinal epithelial cells were significantly higher than in the liver. These findings identify intestinal epithelial cells as likely preferential targets for arsenic toxicity and support further studies on the functional consequences of intestinal HO-1 induction.

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Arsenic exposure induced renal fibrosis via regulation of mitochondrial dynamics and the NLRP3‐TGF‐β1/SMAD signaling pathway

Ren,

Li,

et al. 2024

Environmental Toxicology

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Environmental arsenic exposure is one of the major global public health problems. Studies have shown that arsenic exposure can cause renal fibrosis, but the underlying mechanism is still unclear. Integrating the in vivo and in vitro models, this study investigated the potential molecular pathways for arsenic‐induced renal fibrosis. In this study, SD rats were treated with 0, 5, 25, 50, and 100 mg/L NaAsO2 for 8 weeks via drinking water, and HK2 cells were treated with different doses of NaAsO2 for 48 h. The in vivo results showed that arsenic content in the rats' kidneys increased as the dose increased. Body weight decreased and kidney coefficient increased at 100 mg/L. As a response to the elevated NaAsO2 dose, inflammatory cell infiltration, renal tubular injury, glomerular atrophy, tubulointerstitial hemorrhage, and fibrosis became more obvious indicated by HE and Masson staining. The kidney transcriptome profiles further supported the protein–protein interactions involved in NaAsO2‐induced renal fibrosis. The in vivo results, in together with the in vitro experiments, have revealed that exposure to NaAsO2 disturbed mitochondrial dynamics, promoted mitophagy, activated inflammation and the TGF‐β1/SMAD signaling pathway, and finally resulted in fibrosis. In summary, arsenic exposure contributed to renal fibrosis via regulating the mitochondrial dynamics and the NLRP3‐TGF‐β1/SMAD signaling axis. This study presented an adverse outcome pathway for the development of renal fibrosis due to arsenic exposure through drinking water.

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Determination of arsenicals in mouse tissues after simulated exposure to arsenic from rice for sixteen weeks and the effects on histopathological features

Cited by 23 publications

References 52 publications

Effects of Intestinal Microbiota on the Biological Transformation of Arsenic in Zebrafish: Contribution and Mechanism

Effects of Intestinal Microbiota on the Biological Transformation of Arsenic in Zebrafish: Contribution and Mechanism

Differential Effects of Arsenic in Drinking Water on Mouse Hepatic and Intestinal Heme Oxygenase-1 Expression

Arsenic exposure induced renal fibrosis via regulation of mitochondrial dynamics and the NLRP3‐TGF‐β1/SMAD signaling pathway

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