Aluminum trichloride impairs bone and downregulates Wnt/β-catenin signaling pathway in young growing rats

Igwenagu

Interdisciplinary Toxicology

2019

254

149

Aluminium (Al) is frequently accessible to animal and human populations to the extent that intoxications may occur. Intake of Al is by inhalation of aerosols or particles, ingestion of food, water and medicaments, skin contact, vaccination, dialysis and infusions. Toxic actions of Al induce oxidative stress, immunologic alterations, genotoxicity, pro-inflammatory effect, peptide denaturation or transformation, enzymatic dysfunction, metabolic derangement, amyloidogenesis, membrane perturbation, iron dyshomeostasis, apoptosis, necrosis and dysplasia. The pathological conditions associated with Al toxicosis are desquamative interstitial pneumonia, pulmonary alveolar proteinosis, granulomas, granulomatosis and fibrosis, toxic myocarditis, thrombosis and ischemic stroke, granulomatous enteritis, Crohn’s disease, inflammatory bowel diseases, anemia, Alzheimer’s disease, dementia, sclerosis, autism, macrophagic myofasciitis, osteomalacia, oligospermia and infertility, hepatorenal disease, breast cancer and cyst, pancreatitis, pancreatic necrosis and diabetes mellitus. The review provides a broad overview of Al toxicosis as a background for sustained investigations of the toxicology of Al compounds of public health importance.

Section: Toxic Action or Effect Selected Referencesmentioning

confidence: 99%

Section: Toxic Action or Effect Selected Referencesmentioning

confidence: 99%

Aluminium toxicosis: a review of toxic actions and effects

Igwenagu

Interdisciplinary Toxicology

2019

254

149

“…The bone stimulatory growth factors has been inhibited by Al exposure in rats (Li et al, 2015). The bone has been impaired by AlCl3 through downregulation of the Wnt/β-catenin signaling pathway in vivo in young growing rats (Sun et al, 2015). The rat osteoblastic differentiation and mineralization in vitro has been inhibited through Wnt/β-catenin signaling pathway (Cao et al, 2016), and TGF-β1/Smad signaling pathway (Sun et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 alleviates aluminum chloride-induced rat osteoblasts dysfunction

Zhu

Zheng

et al. 2016

Toxicology

Self Cite

Osteoblasts dysfunction, induced by aluminum (Al), plays a critical role in the osteoporosis etiology. Ginsenoside Rb1 (Rb1) has the therapeutic properties for osteoporosis. This study aimed to assess the efficiency of Rb1 in ameliorating Al-induced osteoblasts dysfunction. The osteoblasts were divided into four groups: Rb1-treated group (RG, 0.0145mg/mL Rb1), control group (CG, 0), AlCl-treated group (AG, 0.126mg/mL AlCl·6HO), AlCl+Rb1-treated group (ARG, 0.0145mg/mL Rb1 and 0.126mg/mL AlCl·6HO). After 24h of culture, the osteoblasts viability, the transforming growth factor-β1 (TGF-), bone morphogenetic protein-2 (BMP-2), the insulin-like growth factor I (IGF-I), core-binding factor α1 (Cbfα1) mRNA expressions, glutathione perioxidase (GSH-P and superoxide dismutase (SOD) activities, and reactive oxygen species (ROS) concentration were determined. The osteoblasts ultrastructural features were also observed. In the ARG, the osteoblasts viability, TGF-, BMP-2, IGF-I and Cbfα1 mRNA expressions and the GSH-P and SOD activities were significantly increased, the ROS concentration was significantly decreased, and osteoblasts histology lesion was attenuated compared with the AG. These results demonstrated that Rb1 could significantly reverse osteoblasts viability and osteoblasts growth regulation factor, inhibit oxidative stress, and attenuate histology lesion in the osteoblasts with AlCl. These results indicate that Rb1 can effectively alleviate the AlCl-induced osteoblasts dysfunction.

Environmental Toxicology and Pharmacology

“…Bone formation has been disrupted by Al accumulation, and which causes bone disease (Li et al, 2011;Aaseth et al, 2012). The rat femora has been impaired by AlCl 3 through inhibiting the Wnt/β-catenin signaling pathway in young growing rats (Sun et al, 2015). The bone mineral density and femoral ultrastructure have been decreased and damaged by AlCl 3 (Sun et al, 2016a).…”

Section: Introductionmentioning

confidence: 99%

The suppressive effects of aluminum chloride on the osteoblasts function

Zhu

Yan

et al. 2016

Self Cite

Aluminum (Al) exposure impairs bone formation, and bone formation is mediated by the osteoblasts. But effects of Al on the osteoblasts function remain elusive. The osteoblasts were exposed to 0, 0.0252, 0.126, 0.252mg/mL AlCl·6HO for 24h. The osteoblasts viability, TGF-β, BMP-2, IGF-I and Cbfα1 mRNA expressions, and GSH-P and SOD activities, ROS concentration were determined. The osteoblasts ultrastructural features were also observed. The results showed that AlCl suppressed the osteoblasts viability, TGF-β, BMP-2, IGF-I and Cbfα1 mRNA expressions, GSH-P and SOD activities, and elevated ROS concentration compared with the CG. The ultrastructural features of osteoblasts in the HG showed mitochondrial swelling, foam-like structure, uneven distribution of chromatin, incomplete cell membrane and cytoplasm spillover compared with the CG. It indicates that AlCl inhibits osteoblasts viability, growth regulation factors mRNA expressions, anti-oxidative function, and damaged the osteoblasts histology structure, impairing the osteoblasts function.