Search

Aluminum (Al) is a recognized environmental pollutant that causes neuroinflammatory lesions, leading to neurodegenerative diseases. Interleukin-1 (IL-1) signaling pathway is responsible for regulating inflammatory lesions. However, it remains unclear whether IL-1 signaling pathway is involved in neuroinflammatory lesions induced by Al exposure. In the present study, one hundred and twenty Wistar rats were orally exposed to 0, 50, 150 and 450 mg/kg BW/d aluminum trichloride (AlCl 3 ) for 90 days, respectively. We found that AlCl 3 exposure increased hippocampal Al concentration, reduced hippocampus coefficient, impaired cognitive ability, deteriorated microstructure of hippocampal CA1 and CA3 regions, increased reactive oxygen species (ROS) level, activated astrocytes and microglia, increased pro-inflammatory cytokines contents and mRNA expressions, and decreased anti-inflammatory cytokines contents and mRNA expressions in the hippocampus. These results indicated that AlCl 3 induced the hippocampal inflammatory lesion (HIL). Moreover, AlCl 3 exposure increased the mRNA and protein expression of IL-1 signaling pathway core components in the hippocampus, demonstrating that AlCl 3 activated IL-1 signaling pathway. Furthermore, the correlation between interleukin-1β (IL-1β) content and HIL and activation of the IL-1 signaling pathway was analyzed. Results showed that IL-1β content was positively correlated with pro-inflammatory cytokines contents and mRNA expressions and activation of IL-1 signaling pathway, and was negatively correlated with hippocampus coefficient, anti-inflammatory cytokines contents and mRNA expressions, and the number of hippocampal neurons. The above results demonstrate that AlCl 3 -induced HIL is associated with IL-1 signaling pathway, in which IL-1β is a link., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The aim of this experiment is to explore the effects of aluminum chloride (AlCl 3 ) on the ATPase enzymes and gonadotropin receptors in the testes. Eighty male Wistar rats were orally exposed to 0 mg/kg body weight (BW) (control group, CG), 64 mg/kg BW (low-dose group, LG), 128 mg/kg BW (mid-dose group, MG), or 256 mg/kg BW (high-dose group, HG) for 120 days. The microstructure and ultrastructure of testes; the activities of Na + -K + -ATPase, Mg 2+ -ATPase, and Ca 2+ -ATPase; and the mRNA and protein expressions of follicle-stimulating hormone receptor (FSHR) and luteinizing hormone receptors (LHR) in the testes were examined. The results showed that the testes histological structure were damaged; the activities of Na + -K + -ATPase, Mg 2+ -ATPase, and Ca 2+ -ATPase, the mRNA and protein expressions of FSHR and LHR in the testes were all decreased in the rats with AlCl 3 exposure. It indicates that AlCl 3 causes the dysfunction of testes in rats.

Exposure to aluminum (Al) inhibits bone formation, the principal mechanism possibly due to oxidative stress. However, little data is available that establishes the precise relationship. In this study, Wistar rats were exposed to 0 (GC), 0.4 (GL), 0.8 (GM) or 1.6 (GH) mg/L aluminum trichloride (AlCl 3 ) in drinking water for 90 days, respectively. The concentrations of Al in serum and bone, serum markers of bone metabolism, bone mineral density (BMD) and body weight were measured. Histological changes within femurs were observed by H&E, ALP, and TRACP staining. Oxidative stress markers and JNK apoptotic pathway were detected in bone. The results indicate that AlCl 3 exposure decreased BMD, numbers of ALP-positive osteoblasts and serum levels of bone formation markers (B-ALP, PICP and BGP), and caused damaged to the trabecular structure. Serum levels of bone resorption markers (TRACP-5b, CTX-I) and numbers of TRACP-positive osteoclasts increased in GL, but conversely, they decreased in GM and GH. In addition, AlCl 3 caused oxidative stress, up-regulated expression of c-Jun and pro-apoptotic factors with increased p-JNK/JNK ratio and down-regulated expression of anti-apoptotic factor Bcl-2 in bone. Taken together, these results indicate that bone impairment caused by AlCl 3 is associated with activation of the oxidative stress-mediated JNK apoptotic pathway., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Aluminum (Al) is known to exert hepatotoxicity. However, the mechanisms mostly are unclear. Liver is a metabolism organ that maintains the energy level and structural stability of body, mitochondria are the main sites of energy metabolism, thus, we hypothesized that mitochondrial energy metabolism disorder contributes to liver dysfunction in aluminum chloride (AlCl 3 ) treatment rat. To verify the hypothesis, forty male Wistar rats were randomly allocated and orally exposed to 0, 64mg/kg, 128mg/kg and 256mg/kg body weight AlCl 3 in drinking water for 120days, respectively. We found that AlCl 3 exposure reduced the electron transport chain complexes I-V activities and adenosine triphosphate (ATP) level, as well as disturbed mitochondrial DNA transcript, presenting as the inhibited mRNA expressions of NADH dehydrogenase 1, NADH dehydrogenase 2, cytochrome b, cytochrome c oxidase subunit 1, cytochrome c oxidase subunit 3 and ATP synthase 6, indicating that AlCl 3 exposure disturbs the mitochondrial energy metabolism, and it caused an increase in liver enzymes (Aspartate aminotransferase and Alanine aminotransferase) and histopathological lesions. Additionally, we found that reactive oxygen species accumulation and decreased superoxide dismutase activity in mitochondria, and increased 8-Hydroxydeoxyguanosine levels in mitochondrial DNA, demonstrating AlCl 3 exposure promotes mitochondrial oxidative stress, which may be a contributing factor to mitochondrial energy metabolism disorder and liver dysfunction. The study displayed that mitochondria are the potential target of liver damage induced by AlCl 3 , providing considerable direction for the prevention and clinical intervention of liver diseases., (Copyright © 2017. Published by Elsevier Inc.)