scholarly journals Protective Effect of Fermented Soybean Dried Extracts against TPA-Induced Oxidative Stress in Hairless Mice Skin

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Sandra R. Georgetti ◽  
Rúbia Casagrande ◽  
Fabiana T. M. C. Vicentini ◽  
Marcela M. Baracat ◽  
Waldiceu A. Verri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chemical Properties ◽  
Gas Temperature ◽  
Drying Process ◽  
Hairless Mice ◽  
Total Polyphenol ◽  
Biochemical Alterations ◽  
Soybean Extract ◽  
A Minor

This study evaluated the chemical properties (polyphenol and genistein contents) of soybean extracts obtained by biotransformation and dried by spray dryer at different conditions and theirin vivoability to inhibit 12-O-tetradecanoylphorbol-13-acetate- (TPA-) induced biochemical alterations in the skin of hairless mice. By comparing the obtained data with that of the well-known active soybean extract Isoflavin beta, we evaluated the influence of the fermentation and drying process in the extracts efficacy. The results demonstrated that inlet gas temperature and adjuvant concentration for the extract drying process have significantly affected the total polyphenol contents and, to a minor degree, the genistein contents. However, the effect of topical stimulus with TPA, an oxidative stress inducer, which caused significant depletion of reduced glutathione (GSH) and catalase, with increased levels of H2O2and lipid peroxidation (MDA) in the skin of hairless mice, was significantly prevented by the soybean extracts treatment. These results indicate that the spray drying processing resulted in a product capable of limiting the oxidative stress with possible therapeutic applicability as an antioxidant in pharmaceutical forms.

Hexagonal boron nitride nanoparticles trigger oxidative stress by modulating thiol/disulfide homeostasis

2021 ◽  
pp. 096032712110028
Author(s):  
F Kar ◽  
İ Söğüt ◽  
C Hacıoğlu ◽  
Y Göncü ◽  
H Şenturk ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Boron Nitride ◽  
Hexagonal Boron Nitride ◽  
Chemical Properties ◽  
Heart Tissue ◽  
Albino Rats ◽  
Dependent Manner ◽  
Tissue Samples ◽  
Boron Nitride Nanoparticles

Background: Hexagonal boron nitride nanoparticles (hBN NPs) are encouraging nanomaterials with unique chemical properties in medicine and biomedical fields. Until now, the optimal hBN NP’s dosage and biochemical mechanism that can be used for in vivo systems has not been fully revealed. The main aim of this article is to reveal characteristics, serum and tissue interactions and any acute cytotoxic effect of different dose of hBN NPs for the first time. Methods: hBN NPs at concentrations varying between 50–3200 µg/kg was administered by intravenous injection to Wistar albino rats (n = 80) divided into seven dosage and control groups. Blood and tissue samples were taken after 24 hours. Results: Our findings suggested that higher doses hBN NPs caused oxidative stress on the serum of rats dose-dependently. However, hBN NPs did not affect thiol/disulfide homeostasis on kidney, liver, spleen, pancreas and heart tissue of rats. Furthermore, hBN NPs increased serum disulfide formation by disrupting the thiol/disulfide balance in rats. Also, LOOH and MPO levels increased at high doses, while CAT levels decreased statistically. Conclusion: The results revealed that hBN NPs induce oxidative stress in a dose-dependent manner by modulating thiol/disulfide homeostasis in rats at higher concentrations

scholarly journals Nephrotoxicity Evaluation of Indium Phosphide Quantum Dots with Different Surface Modifications in BALB/c Mice

2020 ◽  
Vol 21 (19) ◽  
pp. 7137
Author(s):  
Li Li ◽  
Tingting Chen ◽  
Zhiwen Yang ◽  
Yajing Chen ◽  
Dongmeng Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Biomedical Applications ◽  
Renal Involvement ◽  
Chemical Properties ◽  
Surface Chemical ◽  
Biological Fate ◽  
And Oxidative Stress ◽  
Observation Period

InP QDs have shown a great potential as cadmium-free QDs alternatives in biomedical applications. It is essential to understand the biological fate and toxicity of InP QDs. In this study, we investigated the in vivo renal toxicity of InP/ZnS QDs terminated with different functional groups—hydroxyl (hQDs), amino (aQDs) and carboxyl (cQDs). After a single intravenous injection into BALB/c mice, blood biochemistry, QDs distribution, histopathology, inflammatory response, oxidative stress and apoptosis genes were evaluated at different predetermined times. The results showed fluorescent signals from QDs could be detected in kidneys during the observation period. No obvious changes were observed in histopathological detection or biochemistry parameters. Inflammatory response and oxidative stress were found in the renal tissues of mice exposed to the three kinds of QDs. A significant increase of KIM-1 expression was observed in hQDs and aQDs groups, suggesting hQDs and aQDs could cause renal involvement. Apoptosis-related genes (Bax, Caspase 3, 7 and 9) were up-regulated in hQDs and aQDs groups. The above results suggested InP/ZnS QDs with different surface chemical properties would cause different biological behaviors and molecular actions in vivo. The surface chemical properties of QDs should be fully considered in the design of InP/ZnS QDs for biomedical applications.

scholarly journals (Z)-5-(2,4-Dihydroxybenzylidene)thiazolidine-2,4-dione Prevents UVB-Induced Melanogenesis and Wrinkle Formation through Suppressing Oxidative Stress in HRM-2 Hairless Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Bonggi Lee ◽  
Kyoung Mi Moon ◽  
Seong Jin Kim ◽  
So Hee Kim ◽  
Dae Hyun Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Collagen Fiber ◽  
Enzyme Linked Immunosorbent Assay ◽  
Molecular Signaling ◽  
Dorsal Skin ◽  
Hairless Mice ◽  
Protein Levels ◽  
Uvb Exposure

Background. Uncontrolled melanogenesis and wrinkle formation are an indication of photoaging. Our previous studies demonstrated that (Z)-5-(2,4-dihydroxybenzylidene)thiazolidine-2,4-dione (MHY498) inhibited tyrosinase activity and melanogenesisin vitro.Objective. To examinein vivoeffects of MHY498 as an antiaging compound on UVB-induced melanogenesis and wrinkle formation, we topically applied MHY498 on dorsal skin of HRM-2 hairless mice.Methods. Using histological analysis, we evaluated effects of MHY498 on melanogenesis and wrinkle formation after UVB exposure. In addition, related molecular signaling pathways were examined using western blotting, fluorometric assay, and enzyme-linked immunosorbent assay.Results. MHY498 suppressed UVB-induced melanogenesis by inhibiting phosphorylation of CREB and translocation of MITF protein into the nucleus, which are key factors for tyrosinase expression. Consistently, tyrosinase protein levels were notably reduced in the dorsal skin of the hairless mice by MHY498 treatment. Furthermore, MHY498 inhibited UVB-induced wrinkle formation and collagen fiber destruction by increasing type 1 procollagen concentration and decreasing protein expression levels of MMPs, which play an essential role in collagen fiber degradation. As a mechanism, MHY498 notably ameliorated UVB-induced oxidative stress and NF-κB activation in the dermal skin of the hairless mice.Conclusion. Our study suggests that MHY498 can be used as a therapeutic or cosmetic agent for preventing uncontrolled melanogenesis and wrinkle formation.

scholarly journals Standardized Edible Bird's Nest Extract Prevents UVB Irradiation-Mediated Oxidative Stress and Photoaging in the Skin

Antioxidants ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 1452
Author(s):  
Ok-Kyung Kim ◽  
Dakyung Kim ◽  
Minhee Lee ◽  
Seong-Hoo Park ◽  
Wakana Yamada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ultraviolet B ◽  
Type I ◽  
Ceramide Synthase ◽  
Hairless Mice ◽  
In Vivo Models ◽  
Uvb Irradiation ◽  
Edible Bird’S Nest

We investigated whether standardized edible bird’s nest extract (BNE-PK) can prevent ultraviolet B (UVB) irradiation-mediated oxidative stress and photoaging in the skin using in vitro and in vivo models. BNE-PK increased skin hydration by hyaluronic acid synthesis and activation of ceramide synthase in UVB-irradiated hairless mice and HaCaT cells. Furthermore, BNE-PK suppressed melanogenesis by down-regulation of the cAMP/PKA/CREB/MITF/TRP-1/TRP-2/tyrosinase pathway in UVB-irradiated hairless mice and 3-isobutyl-1-methylxanthine (IBMX)-treated B16F10 cells. In UVB-irradiated hairless mice, BNE-PK attenuated the wrinkle formation-related JNK/c-FOS/c-Jun/MMP pathway and activated the TGF-βRI/SMAD3/pro-collagen type I pathway during UVB-mediated oxidative stress. Based on these findings, our data suggest that BNE-PK may potentially be used for the development of effective natural anti-photoaging functional foods for skin health.

scholarly journals Antioxidant and Anti-Inflammatory Effects of Shungite against Ultraviolet B Irradiation-Induced Skin Damage in Hairless Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Ma. Easter Joy Sajo ◽  
Cheol-Su Kim ◽  
Soo-Ki Kim ◽  
Kwang Yong Shim ◽  
Tae-Young Kang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dorsal Side ◽  
Ultraviolet B ◽  
Mouse Serum ◽  
Molecular Signaling ◽  
Skin Damage ◽  
Proinflammatory Response ◽  
Hairless Mice ◽  
Anti Inflammatory

As fullerene-based compound applications have been rapidly increasing in the health industry, the need of biomedical research is urgently in demand. While shungite is regarded as a natural source of fullerene, it remains poorly documented. Here, we explored thein vivoeffects of shungite against ultraviolet B- (UVB-) induced skin damage by investigating the physiological skin parameters, immune-redox profiling, and oxidative stress molecular signaling. Toward this, mice were UVB-irradiated with 0.75 mW/cm2for two consecutive days. Consecutively, shungite was topically applied on the dorsal side of the mice for 7 days. First, we found significant improvements in the skin parameters of the shungite-treated groups revealed by the reduction in roughness, pigmentation, and wrinkle measurement. Second, the immunokine profiling in mouse serum and skin lysates showed a reduction in the proinflammatory response in the shungite-treated groups. Accordingly, the redox profile of shungite-treated groups showed counterbalance of ROS/RNS and superoxide levels in serum and skin lysates. Last, we have confirmed the involvement of Nrf2- and MAPK-mediated oxidative stress pathways in the antioxidant mechanism of shungite. Collectively, the results clearly show that shungite has an antioxidant and anti-inflammatory action against UVB-induced skin damage in hairless mice.

Pro- and anti-oxidant parameters in rat liver after short term exposure to hexachlorobenzene

1997 ◽  
Vol 16 (5) ◽  
pp. 257-261 ◽  
Author(s):  
MG Almeida ◽  
F. Fanini ◽  
SC Davino ◽  
AE Aznar ◽  
OR Koch ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Condition ◽  
Liver Lipid ◽  
Thiobarbituric Acid ◽  
Oxidative Stress Condition ◽  
Biochemical Alterations ◽  
Short Term Exposure ◽  
Microsomal Cytochrome P450 ◽  
Glucose 6 Phosphate Dehydrogenase

The association between an in vivo oxidative stress condition of the liver and hepatic porphyria during HCB intoxication is postulated. After 30 days of treatment, HCB (25 mg/kg b.w.) promotes an induction of microsomal cytochrome P450 system, increase in microsomal super oxide anion generation accompanied by increased levels of liver lipid peroxidation, as measured by the production of thiobarbituric acid reactants and by spontaneous visible chemiluminescence. Concomitantly, liver antiox idant defenses are slightly modified, with decreased activity of glutathione peroxidase, superoxide dismutase and glucose-6-phosphate dehydrogenase contributing to an oxidative stress condition of the liver. These liver biochemical alterations are closely related to increased levels of urinary coproporphyrin, plasma AST and ALT activities and to the onset of liver morphological lesions

PRELIMINARY CHARACTERIZATION OF THE 5α-DIHYDROTESTOSTERONE BINDING PROTEIN IN THE EPIDIDYMAL CYTOSOL FRACTION. IN VIVO STUDIES

1972 ◽  
Vol 71 (3) ◽  
pp. 614-624 ◽  
Author(s):  
Vidar Hansson ◽  
Ole Djøseland ◽  
Ellen Reusch ◽  
Synnøve Aasvik
Keyword(s):  
Polyacrylamide Gel Electrophoresis ◽  
Chemical Properties ◽  
Sedimentation Coefficient ◽  
Molecular Size ◽  
In Vivo Studies ◽  
Ventral Prostate ◽  
Cytosol Fraction ◽  
A Minor ◽  
Almost All

ABSTRACT Following the administration of [3H] testosterone to castrated rats in vivo, most of the radioactivity in the epididymal cytosol fraction was bound to macromolecules. The molecular weight of the androgen-macromolecular complexes was determined to about 90 000, and the frictional ratio (f/fo) was 1.62. The sedimentation coefficient was shown to be 4.6 S (± 0.2) and the complex was slightly retarded on a column of Sephadex G-100 (Einstein-Stokes radius 47–48 Å). On polyacrylamide gel electrophoresis it moved as a sharp zone with RF: 0.41. Almost all the radioactivity bound to these macromolecules was identified as 5α-dihydrotestosterone (5α-DHT) (95%) and only a minor part (3–4%) as testosterone. The receptor for 5α-DHT in the epididymal cytosol fraction was in its physico-chemical properties shown to be different from the androgenbinding proteins of the rat ventral prostate, and could not be demonstrated in non-target organs like liver and kidney. The receptor for 5α-DHT in the epididymal cytosol fraction did not form aggregates in hypotonic solutions, and was roughly of the same molecular size both at high and low salt concentrations.

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

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