Preparation of magnetic activated carbon-chitosan nanocomposite for crystal violet adsorption

Ferda Civan Çavuşoğlu,Seher Akan,Ezgi Aleyna Arı,Ezgi Çetinkaya,Elif Çolak,Gamze Nur Daştan,Semina Deniz,Damla Erdem,Melda Köksal,Sevgi Korkmaz,Nursena Onsekiz,Betül Oruçoğlu,Didem Özkaya,Hamdi Buğra 한국화학공학회 2019 Korean Journal of Chemical Engineering Vol.36 No.11

Magnetic, cheap and versatile adsorbents were developed for crystal violet (CV) adsorption in this study. These adsorbents are magnetic activated carbon (AC-Fe3O4) and chitosan grafted magnetic activated carbon (Chitosan- AC-Fe3O4). Fe3O4 and chitosan were also used for adsorption. X-ray diffraction (XRD), scanning electron microscopy (SEM), vibrating sample magnetometer (VSM), zeta potential analysis and Fourier transform infrared spectroscopy (FTIR) methods were used for characterization of adsorbents. Adsorption parameters for CV were investigated. Raw chitosan and Fe3O4 were also used for CV adsorption to compare the results of composites. The chosen adsorption parameters are amount of adsorbent, contact time, initial CV concentration, and temperature. The equilibrium period was observed to be very short for chitosan and Fe3O4 nanoparticles. The adsorption efficiencies of these adsorbents are very low. AC-Fe3O4 and AC-Fe3O4-Chitosan nanoparticles reached equilibrium at 80min. The all adsorbent-CV systems followed pseudo second-order kinetic model. AC-Fe3O4 and AC-Fe3O4-Chitosan composites suited non-linear Freundlich isotherm for all temperatures (298, 308 and 318 K). Regeneration of adsorbents was also investigated. 1M of acetic acid and 0.1M of NaOH solutions were tested. Acetic acid solution desorbed CV better than NaOH solution at 6 hours.

Protective Effect of Ginkgo biloba L. Leaf Extract Against Glyphosate Toxicity in Swiss Albino Mice

Kültiğin Çavuşoğlu,Kürşad Yapar,Ertan Oruç,Emine Yalçın 한국식품영양과학회 2011 Journal of medicinal food Vol.14 No.10

The aim of the present study was to investigate the protective role of Ginkgo biloba L. leaf extract against the active agent of Roundup^ⓡ herbicide (Monsanto, Creve Coeur, MO, USA). The Swiss Albino mice were randomly divided into six groups, with each group consisting of six animals: Group I (control) received an intraperitoneal injection of dimethyl sulfoxide (0.2 mL, once only), Group II received glyphosate at a dose of 50 mg/kg of body weight, Group III received G. biloba at a dose of 50 mg/kg of body weight, Group IV received G. biloba at a dose of 150 mg/kg of body weight, Group V received G. biloba (50 mg/kg of body weight) and glyphosate (50 mg/kg of body weight), and Group VI received G. biloba (150 mg/kg of body weight) and glyphosate (50 mg/kg of body weight). The single dose of glyphosate was given intraperitoneally. Animals from all the groups were sacrificed at the end of 72 hours, and their blood, bone marrow, and liver and kidney tissues were analyzed for aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine, malondialdehyde (MDA), and glutathione (GSH) levels and the presence of micronucleus (MN), chromosomal aberrations (CAs), and pathological damages. The results indicated that serum AST, ALT, BUN, and creatinine levels significantly increased in mice treated with glyphosate alone compared with the other groups (P<.05). Besides, glyphosate-induced oxidative damage caused a significant decrease in GSH levels and a significant increase in MDA levels of the liver and kidney tissues. Moreover, glyphosate alone–treated mice presented higher frequencies of CAs, MNs, and abnormal metaphases compared with the controls (P<.05). These mice also displayed a lower mean mitotic index than the controls (P<.05). Treatment with G. biloba produced amelioration in indices of hepatotoxicity, nephrotoxicity, lipid peroxidation, and genotoxicity relative to Group II. Each dose of G. biloba provided significant protection against glyphosate-induced toxicity, and the strongest effect was observed at a dose of 150 mg/kg of body weight. Thus, in vivo results showed that G. biloba extract is a potent protector against glyphosate-induced toxicity, and its protective role is dose-dependent.

Royal Jelly (Honey Bee) Is a Potential Antioxidant Against Cadmium-Induced Genotoxicity and Oxidative Stress in Albino Mice

Kültiğin Çavuşoğlu,Kürşad Yapar,Emine Yalçin 한국식품영양과학회 2009 Journal of medicinal food Vol.12 No.6

Cadmium (Cd) is a highly toxic heavy metal that induces genotoxic damage in the body. Besides, Cd induces oxidative damage in various tissues by altering antioxidant defence enzymes system. In this study, we investigated the protective role of royal jelly (RJ) on Cd-induced genotoxicity and oxidative stress in mice. For this aim, the micronucleus (MN) test in erythrocytes and exfoliated cells of buccal mucosa and the chromosome aberration (CA) test in bone marrow cells were applied. In addition, the levels of reduced glutathione (GSH) and malondialdehyde (MDA) were evaluated in the liver and kidneys. Thirty-six animals were divided into six groups: the control group received distilled water alone, whereas mice in the treatment groups received RJ alone (100 and 250mg/kg of body weight), Cd alone (2mg/kg of body weight), and RJ+Cd. Cd toxicity resulted in a significant (P<.05) increase in CAs, abnormal metaphase number, and MN formation. Cd also caused a decrease in mitotic index. Oral administration of RJ at two doses (100 and 250mg/kg of body weight) showed significant (P<.05) suppression of mutagenic effects of Cd. Moreover, Cd-induced oxidative damage caused a significant decrease in GSH level and a significant increase in MDA level in the liver and kidneys. Treatment with two doses of RJ caused a significant recovery in antioxidant status of GSH and a significant inhibition of MDA production. It could be concluded that RJ has a protective role against Cd-induced genotoxicity and oxidative stress in mice, due to its antioxidant effects.

The Protective Effect of Royal Jelly on Chronic Lambda-Cyhalothrin Toxicity: Serum Biochemical Parameters, Lipid Peroxidation, and Genotoxic and Histopathological Alterations in Swiss Albino Mice

Kültiğin Çavuşoğlu,Kürşad Yapar,Ertan Oruç,Emine Yalçın 한국식품영양과학회 2011 Journal of medicinal food Vol.14 No.10

The present study was undertaken to investigate the protective effect of royal jelly (RJ) against toxicity induced by a synthetic pyrethroid insecticide, lambda-cyhalothrin (LCT), in Swiss albino mice. Animals were randomly divided into six groups of six animals each. The control group received distilled water alone, whereas mice in the treatment groups received RJ alone (100 or 250 mg/kg of body weight), LCT alone (668 ppm), or RJ+LCT for 21 days. All mice (100%) survived until the end of experiment and were sacrificed at the end of 24 hours. Blood, bone marrow, and liver and kidney tissues were analyzed for aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine, malondialdehyde (MDA), and reduced glutathione (GSH) levels and micronucleus (MN) frequency, chromosomal aberrations (CAs), and pathological damages. Serum AST, ALT, BUN, and creatinine levels were elevated in mice treated with LCT alone compared with the other tested groups (P<.05). LCT-induced oxidative damage caused a significant decrease in GSH levels and a significant rise in MDA levels of liver and kidney tissues. LCT alone–treated mice presented higher frequencies (P<.05) of MNs, CAs, and abnormal metaphases compared with the controls; moreover, the mitotic index was lower than in controls (P<.05). Oral treatment with RJ significantly ameliorated the indices of hepatotoxicity, nephrotoxicity, lipid peroxidation, and genotoxicity induced by LCT. Both doses of RJ tested provided significant protection against LCT-induced toxicity, and its strongest effect was observed at the dose level of 250 mg/kg of body weight. In vivo results suggest that RJ is a potent antioxidant against LCT-induced toxicity, and its protective effect is dose dependent.

Protective Effect of Royal Jelly and Green Tea Extracts Effect Against Cisplatin-Induced Nephrotoxicity in Mice: A Comparative Study

Kürşad Yapar,Kültiğin Çavuşoğlu,Ertan Oruç,Emine Yalçin 한국식품영양과학회 2009 Journal of medicinal food Vol.12 No.5

The aim of the present study was to investigate the protective role of royal jelly (RJ) and green tea (GT) extracts on cisplatin (cDDP)-induced nephrotoxicity in adult albino mice. Albino mice were randomly divided into six groups: Group I (control) received a single intraperitoneal injection of isotonic saline (0.02mL/g), Group II received a single intraperitoneal injection of cDDP (7mg/kg of body weight), Group III received RJ (100mg/kg of body weight), Group IV received GT (100mg/kg of body weight), Group V received RJ (100mg/kg of body weight)+cDDP (7mg/kg of body weight), and Group VI received GT (100mg/kg of body weight)+cDDP (7mg/kg of body weight). The concentrations of blood urea nitrogen (BUN) and creatinine were evaluated. In addition, kidney samples were taken for determination of tissue malondialdehyde (MDA) and reduced glutathione (GSH) levels. In addition, histopathological changes in kidneys were investigated. The results indicated that no significant differences in MDA, GSH, BUN, and creatinine levels were observed among the control group and groups treated with RJ alone and GT alone (P>.05). However, there was a significant increase in BUN and creatinine parameters after cDDP application in Groups II, V, and VI. The mice treated with only cDDP exhibited an increase in serum BUN and creatinine levels when compared to Groups V and VI (P<.05). Moreover, cDDP-induced oxidative damage caused a significant decrease in GSH levels and a significant increase in MDA levels in kidneys (P<.05). RJ and GT supplementation attenuated cDDP-induced nephrotoxicity, which was manifested by stopping the elevation in serum creatinine and BUN levels. Moreover, RJ and GT supplementation restored GSH content and MDA production levels in the kidney tissue following cDDP treatment (P<.05). These products were also effective in protecting against cDDP-induced tissue damage in mouse kidneys. In conclusion, 100mg/kg of body weight doses of RJ and GT provided protection against cDDP-induced nephrotoxicity, and both products can act as protector agents against cDDP-induced kidney damages.

Protective Role of Grape Seed Extract Against Doxorubicin-Induced Cardiotoxicity and Genotoxicity in Albino Mice

Emine Yalçin,Ertan Oruç,Kültiğin Çavuşoğlu,Kürşad Yapar 한국식품영양과학회 2010 Journal of medicinal food Vol.13 No.4

In this study, the protective role of grape seed extract (GSE) against doxorubicin (DOX)-induced cardiotoxicity and genotoxicity has been evaluated in male Mus musculus var. albino mice. The micronucleus (MN) test in erythrocytes and the chromosome aberration (CA) test in bone marrow cells were used. Also, levels of reduced glutathione (GSH) and lipid peroxidation as malondialdehyde (MDA) in heart homogenates were measured, and in addition the changes in heart histology were investigated. The mice were randomly divided into six groups. Group I (negative control) received intraperitoneal injections of isotonic saline (0.02mL/g) for 6 consecutive days, Group II received intraperitoneal injections of DOX (2.5mg/kg of body weight, six doses every other day; cumulative dosage, 15mg/kg of body weight) for 6 consecutive days, Group III received GSE (50mg/kg of body weight, 21 doses every other day; cumulative dosage, 1,050mg/kg of body weight) for 21 consecutive days, Group IV received GSE (150mg/kg of body weight, 21 doses every other day; cumulative dosage, 3,150mg/kg of body weight) for 21 consecutive days, Group V received GSE (50mg/kg of body weight, 28 doses every other day; cumulative dosage, 1,400mg/kg of body weight) for 28 consecutive days plus DOX (2.5mg/kg of body weight, six doses every other day; cumulative dosage, 15mg/kg of body weight) for 6 consecutive days, and Group VI received GSE (150mg/kg of body weight, 28 doses every other day; cumulative dosage, 4,200mg/kg of body weight) for 28 consecutive days plus DOX (2.5mg/kg of body weight, six doses every other day; cumulative dosage, 15mg/kg of body weight) for 6 consecutive days. DOX induced heart damage as indicated from a pronounced change in heart histology. In the DOX-treated group, there was a significant increase in MDA content in the heart homogenate, and the level of GSH was significantly decreased. DOX induced genotoxicity by increasing the number of aberrant metaphases (AMNs), MNs, and structural chromosomal aberrations (CAs) such as chromatid breaks, dicentrics, acentric fragments, and gaps and showed a detractive effect on the mitotic index (MI) of cells. Pretreatment with GSE before treatment with DOX significantly protected the heart tissue by ameliorating its antioxidant activity. In Groups V and VI, the MDA level of heart tissue was significantly decreased, and the GSH level was increased compared to the DOX-treated group. Moreover, GSE significantly protected bone marrow chromosomes from DOX-induced genotoxicity by reducing the total AMNs and the frequency of structural CAs. GSE treatment also decreased the frequency of MNs and increased the MI values. It could be concluded that GSE acts as a potent antioxidant to prevent heart damage and genotoxicity of bone marrow cells.