scholarly journals Protective Effect of Lactobacillus rhamnosus GG on TiO2 Nanoparticles-Induced Oxidative Stress Damage in the Liver of Young Rats

Nanomaterials ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 803
Author(s):  
Penghui Nie ◽  
Mengqi Wang ◽  
Yu Zhao ◽  
Shanji Liu ◽  
Ling Chen ◽  
...  

The potential toxicity of titanium dioxide nanoparticles (TiO2 NPs) to mammals has become a widespread concern. Young individuals exposed to TiO2 NPs have a higher risk than adults. In this study, the protective effects of Lactobacillus rhamnosus GG (LGG) on liver toxicity in young rats induced by TiO2 NPs were explored. Results show that the four-week-old rats that underwent LGG after the oral intake of TiO2 NPs could prevent weight loss, reduce hematological indicators (WBC and NEUT) and serum biochemical indicators (AST, ALT, AST/ALT, and ALP). Moreover, it alleviated the pathological damage of the liver (as indicated by the disordered hepatocytes, more eosinophilic, ballooning degeneration, and accompany with blood cells), but it did not reduce the Ti contents in the liver. In addition, RT-qPCR results indicated that LGG restored the expression of anti-oxidative stress-related genes, such as SOD1, SOD2, CAT, HO-1, GSH, GCLC, and GCLM in the liver. In summary, the hepatotoxicity of TiO2 NPs in young rats is closely related to oxidative stress, and the antioxidant effect of LGG might protect the harmful effects caused by TiO2 NPs.

2006 ◽  
Vol 291 (4) ◽  
pp. R927-R935 ◽  
Author(s):  
Susanne Rohrbach ◽  
Stefanie Gruenler ◽  
Mirja Teschner ◽  
Juergen Holtz

Cellular redox balance is maintained by various antioxidative systems. Among those is the thioredoxin system, consisting of thioredoxin, thioredoxin reductase, and NADPH. In the present study, we examined the effects of caloric restriction (2 mo) on the expression of the cytosolic and mitochondrial thioredoxin system in skeletal muscle and heart of senescent and young rats. Mitochondrial thioredoxin reductase (TrxR2) is significantly reduced in aging skeletal and cardiac muscle and renormalized after caloric restriction, while the cytosolic isoform remains unchanged. Thioredoxins (mitochondrial Trx2, cytosolic Trx1) are not influenced by caloric restriction. In skeletal and cardiac muscle of young rats, caloric restriction has no effect on the expression of thioredoxins or thioredoxin reductases. Enforced reduction of TrxR2 (small interfering RNA) in myoblasts under exposure to ceramide or TNF-α causes a dramatic enhancement of nucleosomal DNA cleavage, caspase 9 activation, and mitochondrial reactive oxygen species release, together with reduced cell viability, while this TrxR2 reduction is without effect in unstimulated myoblasts under basal conditions. Oxidative stress in vitro (H2O2in C2C12myoblasts and myotubes) results in different changes: TrxR2, Trx2, and Trx1 are induced without alterations in the cytosolic thioredoxin reductase isoforms. Thus aging is associated with a TrxR2 reduction in skeletal muscle and heart, which enhances susceptibility to apoptotic stimuli but is renormalized after short-term caloric restriction. Exogenous oxidative stress does not result in these age-related changes of TrxR2.


Molecules ◽  
2018 ◽  
Vol 23 (8) ◽  
pp. 1955 ◽  
Author(s):  
Elizabeth Huerta-García ◽  
Iván Zepeda-Quiroz ◽  
Helen Sánchez-Barrera ◽  
Zaira Colín-Val ◽  
Ernesto Alfaro-Moreno ◽  
...  

Titanium dioxide nanoparticles (TiO2 NPs) are widely used in industry and daily life. TiO2 NPs can penetrate into the body, translocate from the lungs into the circulation and come into contact with cardiac cells. In this work, we evaluated the toxicity of TiO2 NPs on H9c2 rat cardiomyoblasts. Internalization of TiO2 NPs and their effect on cell proliferation, viability, oxidative stress and cell death were assessed, as well as cell cycle alterations. Cellular uptake of TiO2 NPs reduced metabolic activity and cell proliferation and increased oxidative stress by 19-fold measured as H2DCFDA oxidation. TiO2 NPs disrupted the plasmatic membrane integrity and decreased the mitochondrial membrane potential. These cytotoxic effects were related with changes in the distribution of cell cycle phases resulting in necrotic death and autophagy. These findings suggest that TiO2 NPs exposure represents a potential health risk, particularly in the development of cardiovascular diseases via oxidative stress and cell death.


Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1698 ◽  
Author(s):  
Antonella Orlando ◽  
Michele Linsalata ◽  
Giusy Bianco ◽  
Maria Notarnicola ◽  
Benedetta D’Attoma ◽  
...  

Celiac disease (CD) is a chronic immune-mediated disorder, characterized by enhanced paracellular permeability across the intestinal epithelium. The complex system of intercellular junctions, including tight junctions (TJs) and adherens junctions (AJs), seals together the epithelial cells to form a continuous layer. The improvements in barrier integrity have been related to modifications in intercellular junction protein expression. Polyamines (spermidine, spermine, and putrescine) actively participate in the modulation of the AJ expression. Both in vitro and in vivo studies have demonstrated that also probiotics can promote the integrity and the function of the intestinal barrier. On these bases, the present work investigated the protective effects exerted by Lactobacillus rhamnosus GG (L.GG) against the pepsin-trypsin-digested gliadin (PTG)-induced enteropathy in jejunal tissue samples of Wistar rats. In particular, the probiotic effects have been evaluated on the intestinal mucosal architecture, polyamine metabolism and intercellular junction protein expression (ZO-1, Occludin, Claudin-1, β-catenin and E-cadherin). The results from this study indicate that L.GG protects the intestinal mucosa of rats from PTG-induced damage, by preventing the reduction of the expression of the intercellular junction proteins. Consequently, a role for L.GG in the therapeutic management of the gluten-related disorders in humans could be hypothesized.


2021 ◽  
Author(s):  
Khurram Shahzad ◽  
Muhammad Naeem Khan ◽  
Farhat Jabeen ◽  
Abdul Shakoor Chaudhry ◽  
Chaman Ara ◽  
...  

Abstract Extensive use of nanotechnology in multiple commodities is raising concern about nanotoxicity and particularly. Particularly, many studies reported the health hazardous effects of titanium dioxide nanoparticles (TiO2-NPs). Study focuses on toxicity and accumulation of TiO2-NPs in tilapia (Oreochromis mossambicus). For this purpose, Tilapia were kept in water tanks, acclimatized for fourteen days, and treated with different doses of TiO2 nanoparticles 0, 0.5, 1.0, and 1.5 mg TiO2-NPs /L. Results revealed an increase in accumulation of TiO2-NPs with an increase in doses. Moreover, with higher dose (1.5 mg /L) gills had maximum levels compared to muscles and liver tissues whereas other doses showed different accumulation patterns. A significantly higher concentration of catalase, glutathione, and lipid peroxidation was recorded in gills (p < 0.05) and superoxide dismutase in the liver. Characteristics like thickening and fusion in lamellae, rupturing of filaments and hyperplasia of gills were also recorded. The phenomenon of increased necrosis and apoptosis in the liver was also noticed with increasing concentration of TiO2-NPs along with formation of sinusoid spaces and condensed nuclear bodies. Elevated values of olive tail movement and % tail DNA were also noticed with increased concentration of TiO2-NPs. This study concluded that TiO2-NPs produced oxidative stress by accumulation in soft tissues and induced pathology and genotoxicity.


Foods ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 986
Author(s):  
Yu Zhao ◽  
Yizhou Tang ◽  
Shanji Liu ◽  
Tiantian Jia ◽  
Donggen Zhou ◽  
...  

The hazard of titanium dioxide nanoparticles (TiO2 NPs) in diseased population should be given focus due to the huge number of these NPs in foods and medicine. This study aimed to evaluate the stronger biological adverse effect of oral exposure to TiO2 NPs in a fructose-induced metabolic syndrome mouse model. Compared to the normal mice, low-dose (2 mg/kg) TiO2 NPs did not cause severe hepatotoxicity. However, high-dose (20 mg/kg) TiO2 NPs induced aggravated hepatic inflammation, fibrosis, and apoptosis, with substantial alteration of related biochemical parameters in the mouse model. Moreover, significantly increased Ti and lipopolysaccharide burden were observed in metabolic syndrome murine liver and serum, which possibly worsened the portend intestinal leakage. The expression of tight junction-related protein showed that TiO2 NPs induced further increase in serious intestinal permeability. The intestinal inflammatory and oxidative stress response in the model were also assessed. Results showed that TiO2 NPs caused more severe intestinal inflammatory injury by intensifying the oxidative stress in metabolic syndrome mice and then induced further liver injury. This work provides information on the insights into the toxic effect of TiO2 NPs in sub-healthy population.


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