Genetic Toxicity of Berberine on Mouse Heart

2014 ◽  
Vol 884-885 ◽  
pp. 634-637
Author(s):  
Cheng Bin Xu ◽  
Lu Wang ◽  
Xiu Juan Hui ◽  
Xi Ping Ma ◽  
Xin Bi ◽  
...  

Berberine, a common drug, which is widely used in clinical medicine as inflammatory medicines, is rarely studied about its affection on non-target organisms in recent researches. To evaluate the eco-toxicity of berberine in mouse heart cells, biochemical responses including oxidative damage and changes in the activities of antioxidative enzymes catalase (CAT), superoxide dismutase (SOD), peroxidase (POD) and malondialdehyde (MDA) induced by berberine were investigated in mouse heart cells. 7.5, 15, 30, 60 and 120 mgkg-1 berberine was added to mouse heart cells respectively. Compared to the controls, the damage, tail DNA content (%) , tail length and tail moment went up respectively in dose-effect manner following the rising berberine; As the content of berberine increased, the activities of SOD, CAT and POD were gradually decreased and the concentration of MDA was gradually increased. Compared to the controls, the change tendency showed significant differences (p<0.05 or p<0.01). In conclusion, berberine induces oxidative stress and DNA damage to heart cells, which may be the significant mechanisms for its toxicity to mice.

2021 ◽  
pp. 096032712110227
Author(s):  
S Kara-Ertekin ◽  
S Yazar ◽  
M Erkan

Pyrethroid pesticides are frequently used for household insect control of insects and in agriculture and livestock. Flumethrin is a pyrethroid that is used against ectoparasites in many animals. The goal of this study was to evaluate the cytotoxic, apoptotic, genotoxic, and estrogenic effects of flumethrin on the mammalian breast cancer cell line (MCF-7). Compared with control groups, a dose-dependent decrease was observed in cell viability at concentrations of 100 µM and higher. The cytotoxic and apoptotic effects detected by LDH assay and AO/EtBr staining increased significantly at a concentration of 1000 µM. The expression of BCL2, which is an anti-apoptotic gene, significantly decreased, whereas BAX, TP53, and P21 expression significantly increased. The results of a comet assay indicated that flumethrin significantly changed tail length, tail % DNA, tail moment, and Olive tail moment in concentrations above 1 and 10 µM. In addition, a 0.1 µM concentration of flumethrin affected ERα receptor mediated cell proliferation and increased transcription of estrogen-responsive pS2 (TFF1) and progesterone receptor (PGR) genes. As a result, flumethrin-induced apoptosis and cytotoxicity at a high concentration, while induced genotoxicity even at lower concentrations. Flumethrin is an endocrine disrupting insecticide with estrogenic effects at very low concentrations.


2017 ◽  
Vol 37 (9) ◽  
pp. 901-908 ◽  
Author(s):  
AM Samir ◽  
LA Rashed

Aim: The aim of this work was to investigate the relationships between aluminium levels, oxidative status and DNA damage in workers occupationally exposed to aluminium. Subjects and methods: This study was conducted in a secondary aluminium smelter. It included 96 male workers occupationally exposed to aluminium fume and dust compared to 96 male nonexposed individuals. Full history and clinical examination were done for all participants. Laboratory investigations in the form of serum aluminium, total antioxidant capacity (TAC), urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG) and comet assay test were performed. Results: Serum aluminium level ranged from 4 to 30 µg/L of median: 10 µg/L; urinary 8-OHdG ranged from 2.7 to 17.2 ng/mg creatinine of median: 7.6 ng/mg creatinine; comet tail length (CTL) ranged from 19.7 to 50.5 µm of median: 45 µm, were statistically significantly increased in the exposed group compared to nonexposed group. In exposed workers, a statistically significant positive correlations were found between serum aluminium level and urinary 8-OHdG ( r = 0.75, p < 0.001); aluminium level and CTL ( r = 0.71, p < 0.001); and urinary 8-OHdG and CTL ( r = 0.71, p < 0.001). There was a statistically significant negative correlation between serum aluminium and TAC ( r = −0.76, p < 0.001). Conclusion: Occupational exposure to aluminium in secondary aluminium smelters was related to the induction of oxidative stress and DNA damage. This may promote the development of adverse health hazards in the exposed workers


Author(s):  
Daihany Moraes Callegari Elaine M. S. G. Lobato

Boron (B) and Calcium (Ca) unbalance in plants during early stages can generate oxidative stress and consequently to interfere negatively on growth and quality of seedlings. This study aims to evaluate the gas exchange and measure the biochemical responses, responding how high concentrations of B and Ca can affect the growth and quality of young Schizolobium parahyba plants. The experimental design used was completely randomised with four treatments [1 - 25 µM B + 5 mM Ca (control); 2 - 25 µM B + 50 mM Ca (Ca high); 3- 250 µM B + 5 mM Ca (B high) and 4 - 250 µM B + 50 mM Ca (B and Ca high)]. Negative impacts on gas exchange, photosynthetic pigments and total glutathione were obtained, besides increases in hydrogen peroxide and electrolyte leakage were verified in plants treated with B and Ca high, indicating oxidative stress. Thus, application 250 µM B combined with 50 mM Ca promoted disorders in plant metabolism, decreasing the growth and quality of young Schizolobium parahyba plants.


2019 ◽  
Vol 2019 ◽  
pp. 1-32 ◽  
Author(s):  
Martha A. Sánchez-Rodríguez ◽  
Víctor Manuel Mendoza-Núñez

Oxidative stress (OS) is the imbalance between oxidant and antioxidant molecules, in favor of oxidants, that causes aging and disease. Many studies have been published that demonstrate the relationship between OS and human health and disease; however, the following questions arise: (i) how are we sure that the OS is present in a biological process? (ii) Is the OS reported in the different investigations equivalent? (iii) What are the best oxidant and antioxidant markers for OS diagnosis? (iv) Can we establish the types and the intensity of the OS? (v) Does OS index could be useful for research and/or application in clinical medicine? In this regard, several indexes have been proposed to measure OS in humans relative to the state of health and disease, among which the following can be highlighted: Oxidative Stress Index (OSI), Tiol Ratios (-SH/TT, -SS/-SH, and-SS/TT), Glutathione Ratio (GSSG/GSH), Oxidative Stress Score (OSS), and OXY-index. Therefore, the aim of this review is to present the state of the art of knowledge about OS indexes for diagnosis of health or disease in humans. We searched for articles in English or Spanish in the PubMed/MEDLINE and Scopus electronic databases published up until May 2019. The keywords used were “oxidative stress,” “index,” and “oxidative stress index.” It was identified 11479 records in both databases, and 490 articles were analyzed. Our review suggests that all indexes analyzed allow diagnose and differentiate the OS related to human health and disease. Also, the studies on OSI, Oxy-score, and OSS indexes have proven to be reliable, practical, and with clinical utility. However, it is necessary to continue with longitudinal studies, especially assess the usefulness of the indexes in the clinical prognosis, and make comparative studies between the different indexes.


Author(s):  
Ramya Dewi Mathialagan ◽  
Zariyantey Abd Hamid ◽  
Qing Min Ng ◽  
Nor Fadilah Rajab ◽  
Salwati Shuib ◽  
...  

Hematopoietic stem/progenitor cells (HSPCs) are susceptible to benzene-induced genotoxicity. However, little is known about the mechanism of DNA damage response affecting lineage-committed progenitors for myeloid, erythroid, and lymphoid. Here, we investigated the genotoxicity of a benzene metabolite, 1,4-benzoquinone (1,4-BQ), in HSPCs using oxidative stress and lineage-directed approaches. Mouse bone marrow cells (BMCs) were exposed to 1,4-BQ (1.25–12 μM) for 24 h, followed by oxidative stress and genotoxicity assessments. Then, the genotoxicity of 1,4-BQ in lineage-committed progenitors was evaluated using colony forming cell assay following 7–14 days of culture. 1,4-BQ exposure causes significant decreases (p < 0.05) in glutathione level and superoxide dismutase activity, along with significant increases (p < 0.05) in levels of malondialdehyde and protein carbonyls. 1,4-BQ exposure induces DNA damage in BMCs by significantly (p < 0.05) increased percentages of DNA in tail at 7 and 12 μM and tail moment at 12 μM. We found crucial differences in genotoxic susceptibility based on percentages of DNA in tail between lineage-committed progenitors. Myeloid and pre-B lymphoid progenitors appeared to acquire significant DNA damage as compared with the control starting from a low concentration of 1,4-BQ exposure (2.5 µM). In contrast, the erythroid progenitor showed significant damage as compared with the control starting at 5 µM 1,4-BQ. Meanwhile, a significant (p < 0.05) increase in tail moment was only notable at 7 µM and 12 µM 1,4-BQ exposure for all progenitors. Benzene could mediate hematological disorders by promoting bone marrow oxidative stress and lineage-specific genotoxicity targeting HSPCs.


Author(s):  
Maher M Khadairi ◽  
Moayed Jy Al-amari ◽  
Ayad Mj Al-mamoori

  Objective: This study determined the effect of purified microcystin-leucine arginine (MC-LR) on biochemical and DNA damage parameters in rats.Methods: Utilization of preparative high-performance liquid chromatography in analysis, purification and collection of MC-LR, then intraperitoneally injection of purified MC-LR to rats. At the end of exposure, animals were sacrificed, and liver cell was isolated to measure the biochemical markers such as superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) as well as measured malondialdehyde (MDA), reactive oxygen species (ROS) and cytochrome P450 (Cyt P450), and DNA damage markers such as comet length, tail length, and tail moment were measured with the single cell gel electrophoresis also called comet assay.Results: The present results showed significantly increased activities of SOD as well as concentration of MDA, ROS with increasing concentration of MC-LR but the activities of CAT and GSH, as well as Cyt P450, were significantly decreased with increasing MC-LR dose while makers of DNA damage such as comet length, tail length, and tail moment also significantly increased with increasing MC-LR dose.Conclusion: This study demonstrated that chronic exposure to MC-LR toxin can induce alteration of biochemical and DNA damage markers.


2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Adam Greasley ◽  
Yanjie Zhang ◽  
Bo Wu ◽  
Yanxi Pei ◽  
Nelson Belzile ◽  
...  

Cardiac hypertrophy is defined as the enlargement of the cardiac myocytes, leading to improper nourishment and oxygen supply due to the increased functional demand. This increased stress on the cardiac system commonly leads to myocardial infarction, contributing to 85% of all cardiac-related deaths. Cystathionine gamma-lyase- (CSE-) derived H2S is a novel gasotransmitter and plays a critical role in the preservation of cardiac functions. Selenocysteine lyase (SCLY) has been identified to produce H2Se, the selenium homologue of H2S. Deficiency of selenium is often found in Keshan disease, a congestive cardiomyopathy. The interaction of H2S and H2Se in cardiac cell hypertrophy has not been explored. In this study, cell viability was evaluated with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Oxidative stress and cell size were observed through immunostaining. The expression of genes was determined by real-time PCR and western blot. Here, we demonstrated that incubation of rat cardiac cells (H9C2) with H2O2 lead to increased oxidative stress and cell surface area, which were significantly attenuated by pretreatment of either H2S or H2Se. H2S incubation induced SCLY/H2Se signaling, which next caused higher expressions and activities of selenoproteins, including glutathione peroxidase and thioredoxin reductase. Furthermore, deficiency of CSE inhibited the expressions of SCLY and selenoprotein P in mouse heart tissues. We also found that both H2S and H2Se stimulated Nrf2-targeted downstream genes. These data suggests that H2S protects against cardiac hypertrophy through enhancement of a group of antioxidant proteins.


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