The suppressive effects of aluminum chloride on the osteoblasts function.

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 AlCl3·6H2O for 24h. The osteoblasts viability, TGF-ß1, BMP-2, IGF-I and Cbfα1 mRNA expressions, and GSH-Px and SOD activities, ROS concentration were determined. The osteoblasts ultrastructural features were also observed. The results showed that AlCl3 suppressed the osteoblasts viability, TGF-ß1, BMP-2, IGF-I and Cbfα1 mRNA expressions, GSH-Px 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 AlCl3 inhibits osteoblasts viability, growth regulation factors mRNA expressions, anti-oxidative function, and damaged the osteoblasts histology structure, impairing the osteoblasts function.

Ginsenoside Rb1 alleviates aluminum chloride-induced rat osteoblasts dysfunction.

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), AlCl3-treated group (AG, 0.126mg/mL AlCl3·6H2O), AlCl3+Rb1-treated group (ARG, 0.0145mg/mL Rb1 and 0.126mg/mL AlCl3·6H2O). After 24h of culture, the osteoblasts viability, the transforming growth factor-ß1 (TGF-ß1), bone morphogenetic protein-2 (BMP-2), the insulin-like growth factor I (IGF-I), core-binding factor α1 (Cbfα1) mRNA expressions, glutathione perioxidase (GSH-Px) 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-ß1, BMP-2, IGF-I and Cbfα1 mRNA expressions and the GSH-Px 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 AlCl3. These results indicate that Rb1 can effectively alleviate the AlCl3-induced osteoblasts dysfunction.

Immunotoxicity of aluminum.

Aluminum (Al) is present in the daily life of all humans. With the incidence of Al contamination increased in recent years, the toxicity of Al on the immune function has attracted more attention. Even with this increased attention, the mechanism of Al immunotoxicity still remains unclear. The mechanism of Al immunotoxicity reviewed herein focused on the effects of Al on the splenic trace elements, the status of α-naphthyl acetate esterase (ANAE) cells, cytokines, complement and immunoglobulins, as well as macrophages. The studies in the literature showed that Al decreased splenic iron (Fe) and zinc (Zn) levels, but the effects of Al on splenic copper (Cu) level was ambiguous and controversial. Al exposure inhibited levels of ANAE(+) cells, the production of interleukin (IL)-2 and the functions of macrophages. With respect to other key cytokines, studies showed that Al suppressed the production of tumor necrosis factor (TNF)-α in vitro; effects of Al on TNF-α formation in vivo were less overt. Al exposure reduced complement 3 (C3) level, but effects of Al exposure on complement 4 (C4) level were not as clear-cut. Lastly, the effects of Al exposure on the IgG, IgM and IgA levels were conflicting. Taken in totality, the results of several studies in the literature demonstrated that Al could impart adverse effects on immune function.

Effects of aluminum trichloride on the trace elements and cytokines in the spleen of rats.

The bioaccumulation and immunotoxicity of aluminum (Al) have been previously documented. Al accumulates in the organs of the organism, including spleen. Spleen is a peripheral organ of the immune system. The accumulated Al may alter the immune function. Here, we investigated the bioaccumulation of Al in spleen and its alterations in the immune system. Forty male Wistar rats (5 weeks old) weighed 110-120 g were orally exposed to aluminum trichloride (AlCl(3)) (0, 64.18, 128.36 and 256.72 mg/kg body weight) in drinking water for 120 days. The concentrations of spleen's Al, iron (Fe), copper (Cu), zinc (Zn), interleukin-2 (IL-2), tumor necrosis factor-α (TNF-α) and growth index were examined at the end of the experiment. The results showed that the concentrations of Al and Cu in the spleen were increased in an AlCl(3)-dose dependent manner, and the concentrations of spleen's growth index, Fe, Zn, IL-2 and TNF-α were reduced in AlCl(3)-treated rats. The results suggest that AlCl(3) can suppress the growth of spleen, disorder the balance of trace elements and inhibit the immune regulation of cytokines in the spleen. It indicates that AlCl(3) suppresses the immune function of spleen.

[Genome sequencing and analysis of the bovine viral diarrhea virus-2 strain JZ05-1 isolated in China].

Bovine viral diarrhea virus (BVDV) is a member of the genus Pestivirus, which is a widespread problem for beef and dairy herds, and has given rise to a significant loss in the livestock industry all over the world. The BVDV strain JZ05-1 isolated from cattle in Jilin, China generated cytopathic effect (CPE) in MDBK cells. Eight overlapped gene fragments were amplified by RT-PCR and sequenced, the complete genom sequence of BVDV strain JZ05-1 was assembled. According to the results, the JZ05-1 genome was composed of 12285 nucleotides in length (GenBank accession No. GQ888686), which could be divided into three regions: a 387 nt 5'-untranslated region (UTR), a 11694 nt single large open reading frame encoding a polyprotein, and a 204 nt 3'-UTR. The 5'-UTR and genome sequences were analyzed by sequence alignment and construction of phylogenetic trees. The strain JZ05-1 was classified as BVDV type 2a. The BVDV-2 strain JZ05-1 genome showed high similarity to the p11Q isolated in Canada and the XJ-04 isolated in China, with 90% and 91% identity in nucleotide sequence, respectively. Compared with the similarity within the BVDV-2 genotype (96%), the JZ05-1 had low sequence similarity to other BVDV-2 strains.

Screening and sequence analysis of the hemolysin gene of Fusobacterium necrophorum.

Fusobacterium necrophorum is the main pathogen that causes numerous necrobacilloses. Hemolysin is one of the major virulence factors involved in fusobacterial infections. In order to investigate the genetic basis of hemolytic activity and the regulation mechanism of the hemolysin expression, a genomic library was constructed from F. necrophorum DNA by ligating DNA fragments generated by partial HindIII digestion with pUC18 vector. The screening of the genomic library with polymerase chain reaction, DNA sequencing and sequence assembly led to a 7.45 kb sequence which includes the putative hly gene and upstream sequence. Clustered putative genes encoding short chain acyl-CoA dehydrogenase (Scad) and electron transfer flavoprotein (Etf) alpha and beta subunits locate upstream of hly. A 535 bp non-coding sequence, possibly with some cis-regulatory elements involved in the regulation of the hemolysin expression in F. necrophorum, locates between etf-beta and hly. The nucleotide sequence of the hly gene indicates it encodes hemolysin. It is the first characterized hemolysin coding gene in F. necrophorum.