Aluminum induced intestinal dysfunction via mechanical, immune, chemical and biological barriers. (February 2022)
- Record Type:
- Journal Article
- Title:
- Aluminum induced intestinal dysfunction via mechanical, immune, chemical and biological barriers. (February 2022)
- Main Title:
- Aluminum induced intestinal dysfunction via mechanical, immune, chemical and biological barriers
- Authors:
- Hao, Wudi
Hao, Chenyu
Wu, Chengrong
Xu, Yuqing
Jin, Cuihong - Abstract:
- Abstract: Aluminum is the most abundant metal element in the Earth's crust, which exists naturally in the form of aluminum compounds. Aluminum is mainly absorbed through the gastrointestinal tract, which varies with different aluminum compounds. During this process, aluminum could induce the disruption of intestinal mucosa barrier. However, its underlying mechanism has not been elucidated yet. Previous studies have reported that aluminum can firstly promote the apoptosis of intestinal epithelial cells, destroy the structure of tight-junction proteins, and increase the intestinal permeability, injuring the mechanical barrier of gut. Also, it can induce the activation of immune cells to secrete inflammatory factors, and trigger immune responses, interfering with immune barrier. Moreover, aluminum treatment can regulate intestinal composition and bio-enzyme activity, impairing the function of chemical barrier. In addition, aluminum accumulation can induce an imbalance of the intestinal flora, inhibit the growth of beneficial bacteria, and promote the proliferation of harmful bacteria, which ultimately disrupting biological barrier. Collectively, aluminum may do extensive damage to intestinal barrier function covering mechanical barrier, immune barrier, chemical barrier and biological barrier. Graphical abstract: Image 1 Highlights: Aluminum was mainly absorbed through gastrointestinal tract, which in turn induce intestinal dysfunction. The absorption of aluminum varies withAbstract: Aluminum is the most abundant metal element in the Earth's crust, which exists naturally in the form of aluminum compounds. Aluminum is mainly absorbed through the gastrointestinal tract, which varies with different aluminum compounds. During this process, aluminum could induce the disruption of intestinal mucosa barrier. However, its underlying mechanism has not been elucidated yet. Previous studies have reported that aluminum can firstly promote the apoptosis of intestinal epithelial cells, destroy the structure of tight-junction proteins, and increase the intestinal permeability, injuring the mechanical barrier of gut. Also, it can induce the activation of immune cells to secrete inflammatory factors, and trigger immune responses, interfering with immune barrier. Moreover, aluminum treatment can regulate intestinal composition and bio-enzyme activity, impairing the function of chemical barrier. In addition, aluminum accumulation can induce an imbalance of the intestinal flora, inhibit the growth of beneficial bacteria, and promote the proliferation of harmful bacteria, which ultimately disrupting biological barrier. Collectively, aluminum may do extensive damage to intestinal barrier function covering mechanical barrier, immune barrier, chemical barrier and biological barrier. Graphical abstract: Image 1 Highlights: Aluminum was mainly absorbed through gastrointestinal tract, which in turn induce intestinal dysfunction. The absorption of aluminum varies with different aluminum compounds. Aluminum disrupted the intestinal barrier system including mechanical, immune, chemical and biological barriers. … (more)
- Is Part Of:
- Chemosphere. Volume 288:Part 2(2022)
- Journal:
- Chemosphere
- Issue:
- Volume 288:Part 2(2022)
- Issue Display:
- Volume 288, Issue 2, Part 2 (2022)
- Year:
- 2022
- Volume:
- 288
- Issue:
- 2
- Part:
- 2
- Issue Sort Value:
- 2022-0288-0002-0002
- Page Start:
- Page End:
- Publication Date:
- 2022-02
- Subjects:
- Aluminum exposure -- Absorption -- Intestinal barrier -- Impairment
AlCl3 aluminum chloride -- AluCi aluminum citrate -- AluP aluminum phosphate -- CAT catalase -- DAO diamine oxidase -- ERK extracellular regulated protein kinases -- GALT gut-associated lymphoid tissues -- GSH glutathione -- HE ematoxylin-eosin -- 5-HT 5-hydroxytryptamine -- IBD inflammatory bowel disease -- IgA immunoglobulin A -- JAMs junctional adhesion molecule -- JECFA the joint Food and Agriculture Organization of the United Nations/World Health Organization Expert Committee on Food Additives -- LDH lactate dehydrogenase -- LPS lipopolysaccharide -- MAPK mitogen-activated protein kinase -- MDA malondialdehyde -- MGG May-Grunwald Giemsa -- MMP9 matrix metalloproteinase-9 -- MPO myeloperoxidase -- MyD88 myeloid differentiation primary response gene 88 -- NAD+ nicotinamide adenine dinucleotide -- NF-κB nuclear factor kappa-B -- NLRP3 nucleotide oligomerization domain-like receptor family pyrin domain containing protein 3 -- NLRs nucleotide oligomerization domain-like receptors -- PAR2 proteinase-activated receptor-2 -- PDH pyruvate dehydrogenase -- ROS reactive oxygen species -- SCFAs Short-chain fatty acids -- SOD superoxide dismutase -- TEER trans-epithelial electrical resistance -- TJs tight junctions -- TLRs Toll-like receptors -- TNF-α tumor necrosis factor-α -- ZO-1 zonula occludens-1.
Pollution -- Periodicals
Pollution -- Physiological effect -- Periodicals
Environmental sciences -- Periodicals
Atmospheric chemistry -- Periodicals
551.511 - Journal URLs:
- http://www.sciencedirect.com/science/journal/00456535/ ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.chemosphere.2021.132556 ↗
- Languages:
- English
- ISSNs:
- 0045-6535
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3172.280000
British Library DSC - BLDSS-3PM
British Library STI - ELD Digital store - Ingest File:
- 20188.xml