The protective role of ascorbic acid on imazalil-induced genetic damage assessed by the cytogenetic tests

2011 ◽  
Vol 28 (7) ◽  
pp. 648-654 ◽  
Author(s):  
Hasan Türkez ◽  
Elanur Aydın
Keyword(s):  
Ascorbic Acid ◽  
Human Lymphocytes ◽  
Protective Role ◽  
Genotoxic Damage ◽  
Metabolic Functions ◽  
Human Peripheral Lymphocytes ◽  
Dose Dependent Decrease ◽  
First Time

Ascorbic acid (AA), known as vitamin C, has important antioxidant and metabolic functions, making its incorporation into the human diet essential. On the other hand, imazalil (IMA), a commonly used fungicide in both agricultural and clinical domains is suspected to produce very serious toxic effects in vertebrates. In this study, the antigenotoxic effects of AA were studied against the genotoxic damage induced by IMA on cultured human lymphocytes using chromosomal aberration (CA) and sister chromatid exchange (SCE) as genetic end points. Human peripheral lymphocytes were treated in vitro with varying concentrations of AA (25, 50, 100, 200, and 400 μg/ml), tested in combination with IMA (336 mg/L). AA alone was not genotoxic and when combined with IMA treatment, reduced the frequencies of CAs and SCEs. A clear dose-dependent decrease in the genotoxic damage of IMA was observed, suggesting a genoprotective role of AA. In conclusion, the preventive role of AA in alleviating IMA-induced DNA damage was indicated for the first time in the present study.

Protective effects of selenium against sister chromatid exchange induced by AFG 1 in human lymphocytes in vitro

2010 ◽  
Vol 30 (6) ◽  
pp. 515-519
Author(s):  
Lokman Alpsoy ◽  
Elif Kotan ◽  
Abdulgani Tatar ◽  
Guleray Agar
Keyword(s):  
Sister Chromatid ◽  
Sister Chromatid Exchange ◽  
Human Lymphocytes ◽  
Protective Role ◽  
Blood Cultures ◽  
Protective Effects ◽  
Low Concentrations ◽  
High Concentrations

Aflatoxins have been shown to be hepatotoxic, carcinogenic, mutagenic and teratogenic to different species of animals. Besides, at low concentrations, Selenium (Se4+) is antimutagenic and anticarcinogenic while it is toxic, mutagenic and carcinogenic at high concentrations. In this study, we aimed to evaluate the effect of Se4+ against aflatoxin GAFG1 (AFG1) on blood cultures in relation to induction of sister chromatid exchange (SCE). The results showed that at 0.4 and 0.8 parts per million (ppm) concentration of AFG1, the frequency of SCE increased in cultured human lymphocytes. When different concentration of Se4+ (0.08 and 8 ppm) were added to AFG1, the frequencies of SCE decreased. Howewer, when 800 ppm concentration of Se4+ together with 0.08 ppm AFG1 were added to cell division inhibited in the cultures. Results suggested that Se4+ could effectively inhibit AFG1-induced SCE. Besides, the protective role of Se4+ against AFG1-induced SCE is probably related to its doses.

scholarly journals Protective role of Eclipta alba L. extract against ethinylestradiol induced genotoxic damage in cultured human lymphocytes

2011 ◽  
Vol 1 (1) ◽  
pp. 4 ◽  
Author(s):  
Yasir Hasan Siddique ◽  
Gulshan Ara ◽  
Tanveer Beg ◽  
Mohammad Faisal ◽  
Mohammad Afzal
Keyword(s):  
Human Lymphocytes ◽  
Metabolic Activation ◽  
Protective Role ◽  
Sister Chromatid Exchanges ◽  
Eclipta Alba ◽  
Replication Index ◽  
Other Substances ◽  
Dose Dependent Decrease ◽  
Chromatid Exchanges

In India, natural preparations derived from plants are widely used for the treatment of various diseases. Hence it becomes necessary to assess the modulating action of the plant extracts when associated with other substances. Ethinylestradiol is not only a genotoxic agent but also a tumor initiating agent. It is widely used in oral contraceptive formulations and also for the treatment of various sexual and metabolic disorders. In the present study, the antigenotoxic effect of Eclipta alba was evaluated against the genotoxic effect induced by 10 μM of ethinylestradiol in the presence of metabolic activation using mitotic index (MI), chromosomal aberrations, sister chromatid exchanges and replication index (RI) as parameters. The treatment of 10 μM of ethinylestradiol along with 1.02x10–4, 2.125x10–4, 3.15x10–4 and 4.17x10–4 g/mL of Eclipta alba (E. alba) extract in culture medium results in a significant dose dependent decrease in the genotoxic effects induced by the treatment of 10 μM of ethinylestradiol. The results of the present study suggest that the plant extract per se does not have genotoxic potential, but can modulate the genotoxicity of ethinylestradiol in cultured human lymphocytes.

Boron Compounds Counteracts Oxidative Stress Mediated Genotoxicity Induced by Fe3O4 Nanoparticles In Vitro

2016 ◽  
Vol 835 ◽  
pp. 84-90 ◽  
Author(s):  
Hasan Türkez ◽  
Erdal Sönmez ◽  
Abdulgani Tatar
Keyword(s):  
Oxidative Stress ◽  
Boric Acid ◽  
Antioxidant Capacity ◽  
Blood Cells ◽  
Defense Mechanisms ◽  
Human Lymphocytes ◽  
Protective Role ◽  
Boron Compounds

Due to rapid growing of nanotechnology, it is currently being used in many areas including biotechnology, electronics, drug delivery systems, cosmetics, material science and biosensors. Oxidative stress is considered as main cause behind the toxicity of nanoparticles (NPs). Recent reports indicate that boron is effective in protecting cells or organisms against oxidative damages by enhancing antioxidant defense mechanisms. However, protective role of boron compounds in nanotoxicity is not investigated yet. Therefore we assessed the potential protective role of boric acid (BA) and borax (BX) against the toxic responses of nano-Fe3O4 particles (IO NPs) in cultured human whole blood cells. Our results showed that IO NPs induced genotoxicity in human lymphocytes demonstrated by sister chromatid exchange (SCE) and 8-hydroxy-2′-deoxyguanosine (8-OH-dG) assays. Again, IO NPs caused decreases of total antioxidant capacity (TAC) and decreases of total oxidative stress (TOS) levels in vitro. Co-application of boric acid and borax (2.5 to 10 ppm) into the cell cultures significantly ameliorated genotoxicity and oxidative stress caused by IO NPs. In a conclusion, this study is the first report revealing that BA and BX significantly protected human blood cells from the toxicity of IO NPs, which is mediated through the generation of oxidative stress and depletion of antioxidant capacity.

scholarly journals An Alternative In Vitro Method for Examining Nanoparticle-Induced Cytotoxicity

2019 ◽  
Vol 38 (5) ◽  
pp. 385-394 ◽  
Author(s):  
Qiang Gu ◽  
Elvis Cuevas ◽  
Syed F. Ali ◽  
Merle G. Paule ◽  
Victor Krauthamer ◽  
...  
Keyword(s):  
Culture Media ◽  
Protective Role ◽  
In Vitro Assays ◽  
Ag Nps ◽  
Validation Data ◽  
Vitro Assay ◽  
Brain Microvessel ◽  
First Time

Conventional in vitro assays are often used as initial screens to identify potential toxic effects of nanoparticles (NPs). However, many NPs have shown interference with conventional in vitro assays, resulting in either false-positive or -negative outcomes. Here, we report an alternative method for the in vitro assessment of NP-induced cytotoxicity utilizing Fluoro-Jade C (FJ-C). To provide proof of concept and initial validation data, Ag-NPs and Au-NPs were tested in 3 different cell cultures including rat brain microvessel endothelial cells, mouse neural stem cells, and the human SH-SY5Y cell line. Conventional 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) and lactate dehydrogenase (LDH) assays were run in parallel with the new method and served as references. The results demonstrate for the first time that FJ-C labeling can be a useful tool for assessing NP-induced cytotoxicity in vitro. Using these approaches, it was also demonstrated that removal of Ag-NPs—while keeping the Ag-ions that were released from the Ag-NPs in culture media—abolished the measured cytotoxicity, indicating that Ag-NPs rather than Ag-ions in solution contributed to the observed cytotoxic effects. Further, co-treatment of Ag-NPs with N-acetyl cysteine (NAC) prevented the observed cytotoxicity, suggesting a protective role of NAC in Ag-NP-induced cytotoxicity. Thus, this alternative in vitro assay is well suited for identify potential cytotoxicity associated with exposure to NPs.

Protective Role of Ascorbic Acid Against Asbestos Induced Toxicity in Rat Lung: In Vitro Study

1990 ◽  
Vol 13 (2-3) ◽  
pp. 249-256 ◽  
Author(s):  
Sikandar G. Khan ◽  
Shahid Ali ◽  
Qamar Rahman
Keyword(s):  
Ascorbic Acid ◽  
In Vitro Study ◽  
Protective Role ◽  
Vitro Study ◽  
Rat Lung

scholarly journals Cathepsin L plays a key role in SARS-CoV-2 infection in humans and humanized mice and is a promising target for new drug development

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Miao-Miao Zhao ◽  
Wei-Li Yang ◽  
Fang-Yuan Yang ◽  
Li Zhang ◽  
Wei-Jin Huang ◽  
...  
Keyword(s):  
Drug Development ◽  
Cathepsin L ◽  
Human Cells ◽  
New Drugs ◽  
Disease Course ◽  
Promising Target ◽  
First Time

AbstractTo discover new drugs to combat COVID-19, an understanding of the molecular basis of SARS-CoV-2 infection is urgently needed. Here, for the first time, we report the crucial role of cathepsin L (CTSL) in patients with COVID-19. The circulating level of CTSL was elevated after SARS-CoV-2 infection and was positively correlated with disease course and severity. Correspondingly, SARS-CoV-2 pseudovirus infection increased CTSL expression in human cells in vitro and human ACE2 transgenic mice in vivo, while CTSL overexpression, in turn, enhanced pseudovirus infection in human cells. CTSL functionally cleaved the SARS-CoV-2 spike protein and enhanced virus entry, as evidenced by CTSL overexpression and knockdown in vitro and application of CTSL inhibitor drugs in vivo. Furthermore, amantadine, a licensed anti-influenza drug, significantly inhibited CTSL activity after SARS-CoV-2 pseudovirus infection and prevented infection both in vitro and in vivo. Therefore, CTSL is a promising target for new anti-COVID-19 drug development.

scholarly journals Secreted KIAA1199 promotes the progression of rheumatoid arthritis by mediating hyaluronic acid degradation in an ANXA1-dependent manner

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wei Zhang ◽  
Guoyu Yin ◽  
Heping Zhao ◽  
Hanzhi Ling ◽  
Zhen Xie ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Hyaluronic Acid ◽  
Dependent Manner ◽  
Collagen Induced Arthritis ◽  
Intracellular Degradation ◽  
Main Pathway ◽  
First Time

AbstractIn inflamed joints, enhanced hyaluronic acid (HA) degradation is closely related to the pathogenesis of rheumatoid arthritis (RA). KIAA1199 has been identified as a hyaladherin that mediates the intracellular degradation of HA, but its extracellular function remains unclear. In this study, we found that the serum and synovial levels of secreted KIAA1199 (sKIAA1199) and low-molecular-weight HA (LMW-HA, MW < 100 kDa) in RA patients were significantly increased, and the positive correlation between them was shown for the first time. Of note, treatment with anti-KIAA1199 mAb effectively alleviated the severity of arthritis and reduced serum LMW-HA levels and cytokine secretion in collagen-induced arthritis (CIA) mice. In vitro, sKIAA1199 was shown to mediate exogenous HA degradation by attaching to the cell membrane of RA fibroblast-like synoviosytes (RA FLS). Furthermore, the HA-degrading activity of sKIAA1199 depended largely on its adhesion to the membrane, which was achieved by its G8 domain binding to ANXA1. In vivo, kiaa1199-KO mice exhibited greater resistance to collagen-induced arthritis. Interestingly, this resistance could be partially reversed by intra-articular injection of vectors encoding full-length KIAA1199 instead of G8-deleted KIAA119 mutant, which further confirmed the indispensable role of G8 domain in KIAA1199 involvement in RA pathological processes. Mechanically, the activation of NF-κB by interleukin-6 (IL-6) through PI3K/Akt signaling is suggested to be the main pathway to induce KIAA1199 expression in RA FLS. In conclusion, our study supported the contribution of sKIAA1199 to RA pathogenesis, providing a new therapeutic target for RA by blocking sKIAA1199-mediated HA degradation.

scholarly journals Arginase Activity in Eisenia andrei Coelomocytes: Function in the Earthworm Innate Response

2021 ◽  
Vol 22 (7) ◽  
pp. 3687
Author(s):  
Joanna Homa ◽  
Alina Klosowska ◽  
Magdalena Chadzinska
Keyword(s):  
Immune Response ◽  
Wound Healing ◽  
Arginase Activity ◽  
Eisenia Andrei ◽  
Heavy Metals Ions ◽  
First Time ◽  
Important Marker

Arginase is the manganese metalloenzyme catalyzing the conversion of l-arginine to l-ornithine and urea. In vertebrates, arginase is involved in the immune response, tissue regeneration, and wound healing and is an important marker of alternative anti-inflammatory polarization of macrophages. In invertebrates, data concerning the role of arginase in these processes are very limited. Therefore, in the present study, we focused on the changes in arginase activity in the coelomocytes of Eisenia andrei. We studied the effects of lipopolysaccharide (LPS), hydrogen peroxide (H2O2), heavy metals ions (e.g., Mn2+), parasite infection, wound healing, and short-term fasting (5 days) on arginase activity. For the first time in earthworms, we described arginase activity in the coelomocytes and found that it can be up-regulated upon in vitro stimulation with LPS and H2O2 and in the presence of Mn2+ ions. Moreover, arginase activity was also up-regulated in animals in vivo infected with nematodes or experiencing segment amputation, but not in fasting earthworms. Furthermore, we confirmed that the activity of coelomocyte arginase can be suppressed by l-norvaline. Our studies strongly suggest that similarly to the vertebrates, also in the earthworms, coelomocyte arginase is an important element of the immune response and wound healing processes.

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