Lycopene: an antioxidant product reducing dithane toxicity in Allium cepa L.

The current study was undertaken to assess the attenuating potential of lycopene against Dithane toxicity in Allium cepa L. roots. A. cepa bulbs were arranged in 6 groups. The control group was treated with tap water while the other groups were treated with 215 mg/L lycopene, 430 mg/L lycopene, 500 mg/L Dithane, 500 mg/L Dithane + 215 mg/L lycopene and 500 mg/L Dithane + 430 mg/L lycopene, respectively. When the treatments were completed, growth inhibition, biochemical, genotoxicity and meristematic cell injury analyses were performed. Lycopene did not cause any toxic effect when applied alone. While rooting percentage, root elongation, weight gain and mitotic index (MI) decreased in response to Dithane exposure, the frequency of micronucleus (MN) and chromosomal abnormalities (CAs) in addition to malondialdehyde (MDA) level and the catalytic activities of superoxide dismutase (SOD) and catalase (CAT) increased. Dithane promoted fragment, sticky chromosome, vagrant chromosome, unequal distribution of chromatin, bridge, nucleus bud and reverse polarization formation in meristem cells. Dithane also provoked meristematic cell injuries, including indistinct appearance of vascular tissue, epidermis cell damage and flattened cell nucleus. Lycopene mitigated all damage types, depending on the lycopene dose applied with Dithane. Hence, the data analysis revealed that lycopene provides exceptional antioxidant protection against the fungicide Dithane, which has devastating toxic potential.

Turmeric (Curcuma longa L.) tends to reduce the toxic effects of nickel (II) chloride in Allium cepa L. roots.

The immense protection potential of plant-derived products against heavy metal toxicity has become a considerable field of research. The goal of the present study was to evaluate the mitigative ability of turmeric against nickel (II) chloride (NiCl2)-related toxicity in the roots of Allium cepa L. For this purpose, one control (treated with tap water) and five treatment groups (treated with 440 mg/L turmeric, 880 mg/L turmeric, 1 mg/L NiCI2, 1 mg/L NiCI2 + 440 mg/L turmeric, and 1 mg/L NiCI2 + 880 mg/L turmeric, respectively) of Allium bulbs were established. Experimental conditions were maintained at room temperature for 3 days. Physiological, biochemical, cytogenetic, and meristematic integrity parameters were analyzed in all groups. NiCl2 reduced germination percentage, root elongation, and weight gain. Following NiCl2 application, the frequency of aberrant chromosomes and micronuclei increased, while mitotic index decreased. NiCl2 caused an increase in oxidative stress, which was evident by increased malondialdehyde level and catalytic activities of superoxide dismutase and catalase. Epidermal and cortex cell injuries as well as deformed cell nuclei and indistinct transmission tissue were observed as a result of NiCl2 treatment. When applied alone, turmeric, which did not cause any negative effects, led to an improvement in all parameters depending on the dose when applied together with NiCl2. Data from the study suggests that turmeric has remarkable protection potential against NiCl2 in Allium cepa.

Molecular docking and toxicity assessment of spirodiclofen: protective role of lycopene.

In this study, toxic effects of spirodiclofen and protective role of lycopene against toxic effects were investigated by using physiological, cytogenetic, anatomical, and biochemical parameters. Allium cepa L. bulbs were used as test material. The bulbs were divided into six groups as one control and five application groups. Bulb in the control group was germinated with tap water, and in treatment groups, 20-mg L-1 dose of spirodiclofen 215- and 430-mg L-1 doses of lycopene were applied. Spirodiclofen application caused a decrease in physiological parameters such as germination percentage, root length, and weight increase. Spirodiclofen administration caused a decrease in the percentage of mitotic index (MI) and an increase in DNA fragmentation, micronucleus (MN), and chromosomal aberration (CA) frequency. Spirodiclofen application caused an increase in the level of the oxidant compound malondialdehyde (MDA), changes in the level of antioxidant enzymes, and disruption of the oxidant/antioxidant balance in the cell. Molecular interactions between spirodiclofen and antioxidant enzymes were determined by molecular docking analysis. In addition to physiological, biochemical, and genetic abnormalities, spirodiclofen also caused deformations in the anatomy of the A. cepa root tip meristematic cells. Lycopene treatment showed a protective effect by suppressing the toxic effects of spirodiclofen, causing a significant improvement in the values of selected physiological, cytogenetic, anatomical, and biochemical parameters. As a result, spirodiclofen insecticide caused toxic effects on various parameters in A. cepa, which is a eukaryotic model organism. In order to elucidate the toxicity mechanism, each parameter is associated with each other. Molecular docking method has revealed the effects of spirodiclofen on antioxidant enzymes. Lycopene application together with spirodiclofen resulted in the regression of all toxic effects and improvement in the root tissue. This result shows that lycopene has a strong protective property against spirodiclofen toxicity.

Hydrogen sulfide dilates the isolated retinal artery mainly via the activation of myosin phosphatase.

AIMS: Hydrogen sulfide (H2S) is shown in ocular tissues and suggested to involve in the regulation of retinal circulation. However, the mechanism of H2S-induced relaxation on retinal artery is not clarified yet. Herein, we aimed to evaluate the role of several calcium (Ca2+) signaling and Ca2+ sensitization mechanisms in the relaxing effect of H2S donor, NaHS, on retinal arteries. MATERIALS AND METHODS: Relaxing effects of NaHS (10-5-3 × 10-3M) were determined on precontracted retinal arteries in Ca2+ free medium as well as in the presence of the inhibitors of Ca2+ signaling and Ca2+ sensitization mechanisms. Additively, Ca2+ sensitivity of the contractile apparatus were evaluated by CaCl2-induced contractions in the presence of NaHS (3 × 10-3M). Functional experiments were furtherly assessed by protein and/or mRNA expressions, as appropriate. KEY FINDINGS: The relaxations to NaHS were preserved in Ca2+ free medium while NaHS pretreatment decreased the responsiveness to CaCl2. The inhibitors of plasmalemmal Ca2+-ATPase, sarcoplasmic-endoplasmic reticulum Ca2+-ATPase, Na+-Ca2+ ion-exchanger and myosin light chain kinase (MLCK) unchanged the relaxations to NaHS. Likewise, Ca2+ sensitization mechanisms including, rho kinase, protein kinase C and tyrosine kinase were unlikely to mediate the relaxation to NaHS in retinal artery. Whereas, a marked reduction was determined in NaHS-induced relaxations in the presence of MLCP inhibitor, calyculin A. Supportively, NaHS pretreatment significantly reduced phosphorylation of MYPT1-subunit of MLCP. SIGNIFICANCE: The relaxing effect of NaHS in retinal artery is likely to be related to the activation of MLCP and partly, to decrement in Ca2+ sensitivity of contractile apparatus.

In vivo protective effects of Ginkgo biloba L. leaf extract against hydrogen peroxide toxicity: cytogenetic and biochemical evaluation.

In this study, the protective effects of Ginkgo biloba leaf extract (GbE) against toxicity induced by hydrogen peroxide (H2O2) in Swiss albino mice were investigated. Abnormal metaphase number (AMn), mitotic index (MI), micronucleus (MN), and chromosomal abnormalities (CAs) were analyzed for cytogenetic effects. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), blood urea nitrogen (BUN), creatinine, glutathione (GSH), and malondialdehyde (MDA) levels in liver and kidney organs were investigated as indicators of biochemical toxicity. Six experimental groups were formed as a control and treatment group, each containing six animals. The mice in the control group were given tap water, while the mice in the administration group received two different doses of GbE and H2O2 for 45 consecutive days. It was observed that H2O2 administration caused a significant decrease in MI compared to the control group and caused a significant decrease in the frequency of AMn, MN, and CAs. Chromatid break was the most common type of CAs induced by H2O2, and the other CAs types observed in this study were chromosome break, fragment, dicentric, gap, and ring. It has been determined that GbE treatment decreases the clastogenic effects of H2O2 and reduces the MN and CAs frequency and causes a re-increase in mitotic cell numbers. It was determined that H2O2 administration caused changes in biochemical parameters and resulted in significant increases in serum AST, ALP, ALT, BUN, and creatinine levels. However, the level of MDA, which is an indicator of oxidative damage, increased, and GSH level decreased in liver and kidney tissues. Oxidative damage caused by H2O2 in liver and kidney tissues was improved, and all biochemical parameters tested were found to be ameliorated after GbE treatment. This improvement was dependent on the dose of GbE, and improvement in 150 mg/kg bw GbE was found to be more prominent. As a result, the GbE can be used as an antioxidant nutritional supplement to protect against the toxic effects of environmental agents such as H2O2.

Ontology-based automatic identification of public health-related Turkish tweets.

Social media analysis, such as the analysis of tweets, is a promising research topic for tracking public health concerns including epidemics. In this paper, we present an ontology-based approach to automatically identify public health-related Turkish tweets. The system is based on a public health ontology that we have constructed through a semi-automated procedure. The ontology concepts are expanded through a linguistically motivated relaxation scheme as the last stage of ontology development, before being integrated into our system to increase its coverage. The ultimate lexical resource which includes the terms corresponding to the ontology concepts is used to filter the Twitter stream so that a plausible tweet subset, including mostly public-health related tweets, can be obtained. Experiments are carried out on two million genuine tweets and promising precision rates are obtained. Also implemented within the course of the current study is a Web-based interface, to track the results of this identification system, to be used by the related public health staff. Hence, the current social media analysis study has both technical and practical contributions to the significant domain of public health.

Physiological, anatomical, biochemical, and cytogenetic effects of thiamethoxam treatment on Allium cepa (amaryllidaceae) L.

In the present study, toxic effects of active substance thiamethoxam of the insecticide Eforia were investigated on Allium cepa L. For this aim, we used the germination percentage, root length, weight gain, malondialdehyde (MDA) level, frequency of micronucleus (MN), chromosomal aberrations (CAs), and mitotic index (MI) as indicators of toxicity. Also, the changes in the root anatomy of A. cepa seeds treated with thiamethoxam were examined. The seeds in all the treatment groups were treated with three different doses (100, 250, and 500 mg/kg) of thiamethoxam for 72 h. The results showed that there were significant alterations in the germination percentage, root length, weight gain, MDA level, MN, CAs, and MI frequency depending on application dose in the seeds exposed to thiamethoxam compared to control group. Thiamethoxam treatments significantly reduced the germination percentage, root length, and weight gain in all the treatment groups (P < 0.05). But, it caused an increase in MN and CAs formation (P < 0.05). It was also found that thiamethoxam has a mito-depressive action on mitosis, and the MI was decreased depending on the dose of applied-thiamethoxam (P < 0.05). About 100, 250, and 500 mg/kg doses of thiamethoxam significantly enhanced the lipid peroxidation and caused an increase in MDA levels at each dose treatment (P < 0.05). Some anatomical damages such as necrotic cell death, unclear vascular tissue, unclear epidermis layer, cell deformation, and unusual form of cell nucleus were observed by using light micrographs. Each dose of thiamethoxam caused severe toxic effects on A. cepa cells, and the maximum toxic effect was observed at the dose level of 500 mg/kg.

Protective effect of Ginkgo biloba L. leaf extract against glyphosate toxicity in Swiss albino mice.

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.

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.

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 role of Ginkgo biloba on petroleum wastewater-induced toxicity in Vicia faba L. (Fabaceae) root tip cells.

The Melet is one of Turkey's economically important rivers. Most of the petroleum plants are located at fairly nearby of the river This situation is considered as main source of heavy metal pollution in the river. The present study was designed to evaluate the protective role of Ginkgo biloba (GB) on cytotoxicity induced by petroleum wastewater in Vicia faba root tip cells. For this aim, we used the germination percentage, root length, weight gain and micronucleus (MN) frequency as indicators of cytotoxicity. Additionally to the cytological analysis, lipid peroxidation analyses were also performed in V. faba roots. Heavy metal concentrations in wastewater were measured by atomic absorption spectrophotometer (AAS). The V. faba seeds were divided into six groups. They were treated with petroleum wastewater and 10, 20 and 30 microM doses of GB. As a result, the mean concentrations of heavy metals in wastewater were observed in the order: Pb > A > Ni > Cr > Fe > Cu > Zn > Cd. The highest germination percentage was observed in the seeds of the control and positive control groups (in proportion as 98 and 96%, respectively). Wastewater treatment caused a significant decrease in the germination percentage of Group III (in proportion as 44%). The highest root length and weight gain were observed in the seeds of the control and positive control groups at the end of the experimental period. The least root length and weight gain were observed in the seeds of Group III treated with wastewater alone. In the control group, the final weights of all the seeds increased about 4.08 g according to initial weight. The root lengths of the control seeds were measured as 6.80 cm at the end of the experimental period. The final weights of the seeds exposed to wastewater alone increased about 0.90 g according to initial weight. Besides, there was a significantly increase in the MDA levels of the roots exposed to wastewater. Heavy metals in wastewater significantly affected the MDA production indicating lipid peroxidation. But, GB-treatment caused amelioration in indices of the germination percentage, root length, weight gain, MN frequency and lipid peroxidation when compared with group III. Each dose of GB provided protection against wastewater toxicity and its strongest protective effect observed at dose of 30 microM. In vivo results showed that GB is a potential protector against toxicity induced by petroleum wastewater and its protective role is dose-dependent.

Protective role of grape seed extract against doxorubicin-induced cardiotoxicity and genotoxicity in albino mice.

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 (0.02 mL/g) for 6 consecutive days, Group II received intraperitoneal injections of DOX (2.5 mg/kg of body weight, six doses every other day; cumulative dosage, 15 mg/kg of body weight) for 6 consecutive days, Group III received GSE (50 mg/kg of body weight, 21 doses every other day; cumulative dosage, 1,050 mg/kg of body weight) for 21 consecutive days, Group IV received GSE (150 mg/kg of body weight, 21 doses every other day; cumulative dosage, 3,150 mg/kg of body weight) for 21 consecutive days, Group V received GSE (50 mg/kg of body weight, 28 doses every other day; cumulative dosage, 1,400 mg/kg of body weight) for 28 consecutive days plus DOX (2.5 mg/kg of body weight, six doses every other day; cumulative dosage, 15 mg/kg of body weight) for 6 consecutive days, and Group VI received GSE (150 mg/kg of body weight, 28 doses every other day; cumulative dosage, 4,200 mg/kg of body weight) for 28 consecutive days plus DOX (2.5 mg/kg of body weight, six doses every other day; cumulative dosage, 15 mg/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.

Protective role of Ginkgo biloba against hepatotoxicity and nephrotoxicity in uranium-treated mice.

The aim of the present study was to investigate the protective role of Ginkgo biloba leaf extract against uranium (U)-induced toxicity in Swiss albino mice. The mice were randomly divided into six groups, each consisting of six animals: Group I (control) received tap water alone, Group II received U at a dose of 5 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 U (5 mg/kg of body weight), and Group VI received G. biloba (150 mg/kg of body weight) and U (5 mg/kg of body weight) by oral gavage for 5 days. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels were determined to assess liver and kidney function, respectively. Also, liver and kidney samples were taken for the determination of tissue malondialdehyde (MDA) and reduced glutathione (GSH) levels, and histopathological changes in liver and kidneys were investigated. The results indicated that there was a significant increase (P < .05) in selected serum parameters. Serum AST, ALT, BUN, and creatinine levels significantly increased in mice treated with U alone when compared to the other groups. Moreover, U-induced oxidative damage caused a significant decrease in GSH levels and a significant increase in MDA levels of liver and kidney tissues. Treatment with G. biloba produced amelioration in biochemical indices of hepatotoxicity and nephrotoxicity according to Group II. Each dose of G. biloba provided significant protection against U-induced toxicity, and its strongest effect was observed at a dose of 150 mg/kg of body weight. In vivo results showed that G. biloba extract is a potent protector against U-induced toxicity, and its protective role is dose-dependent.

Protective effect of kombucha mushroom (KM) tea on phenol-induced cytotoxicity in albino mice.

The present study was carried out to evaluate the protective role of kombucha mushroom (KM) tea on cytotoxicity induced by phenol (PHE) in mice. We used weight gain and micronucleus (MN) frequency as indicators of cytotoxicity and supported these parameters with pathological findings. The animals were randomly divided into seven groups: (Group I) only tap water (Group II) 1000 microl kg(-1) b. wt KM-tea, (Group III) 35 mg kg(-1) body wt. PHE (Group IV) 35 mg kg(-1) body wt. PHE + 250 microl kg(-1) b. wt KM-tea (Group V) 35 mg kg(-1) b. wt PHE + 500 microl kg(-1) b. wt KM-tea (Group VI) 35 mg kg(-1) b. wt PHE + 750 microl kg(-1) b. wt KM-tea, (Group VII) 35 mg kg(-1) b. wt PHE + 1000 microl kg(-1) b. wt KM-tea, for 20 consecutive days by oral gavage. The results indicated that all KM-tea supplemented mice showed a lower MN frequency than erythrocytes in only PHE-treated group. There was an observable regression on account of lesions in tissues of mice supplemented with different doses of KM-tea in histopathological observations. In conclusion, the KM-tea supplementation decreases cytotoxicity induced by PHE and its protective role is dose-dependent.

Protective role of Royal Jelly (honeybee) on genotoxicity and lipid peroxidation, induced by petroleum wastewater, in Allium cepa L. root tips.

In the present study, the protective effect of Royal Jelly (RJ) on genotoxicity and lipid peroxidation, induced by petroleum wastewater, in Allium cepa L. root-tip cells was investigated. For this purpose, we used the malondialdehyde (MDA) level, mitotic index (MI), frequency of micronucleus (MN) and chromosomal aberrations (CAs) as indicators of genotoxicity and lipid peroxidation, and correlated these data with statistical parameters. In additional to the genotoxic analysis, we examined changes in the root anatomy of A. cepa seeds treated with the wastewater. Heavy metal concentrations in the wastewater were measured by atomic absorption spectrophotometry. The seeds were divided into six groups as control, wastewater and RJ treatment groups. They were treated with the wastewater alone, RJ alone (25 and 50 microm doses) and RJ + wastewater for 10 consecutive days. As a result, the mean concentrations of heavy metals in the wastewater were observed to be in the order: Pb > Fe > Al > Ni > Cu > Zn > Cr > Cd. The results showed that there was a significant alteration in MI and in the frequency of MN and CAs in the seeds exposed to the wastewater when compared with the controls. The wastewater exposure resulted in a significant increase in CAs and MN formation (P < 0.05). The wastewater also caused a decrease in MI (P < 0.05). Additionally, there was a significant increase in the MDA levels of the roots exposed to the wastewater (P < 0.05). Heavy metals in the petroleum wastewater significantly increased the MDA production, indicating lipid peroxidation. Moreover, light micrographs showed anatomical damages such as an accumulation of chemical compounds in cortex parenchyma, cell death, an unusual form of cell nucleus and unclear vascular tissue. However, the RJ treatment caused amelioration in the indices of lipid peroxidation and MI, and in the frequency of CAs and MN, when compared with the group treated with petroleum wastewater alone (P < 0.05). Also, the RJ application caused the recuperation of anatomical structural damages induced by the petroleum wastewater. Each dose of RJ provided protection against the wastewater toxicity, and the strongest protective effect was observed at dose of 50 microm. In vivo results showed that RJ is a potential protector against toxicity induced by petroleum wastewater, and its protective role is dose-dependent.

Protective effect of royal jelly and green tea extracts effect against cisplatin-induced nephrotoxicity in mice: a comparative study.

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 (0.02 mL/g), Group II received a single intraperitoneal injection of cDDP (7 mg/kg of body weight), Group III received RJ (100 mg/kg of body weight), Group IV received GT (100 mg/kg of body weight), Group V received RJ (100 mg/kg of body weight) + cDDP (7 mg/kg of body weight), and Group VI received GT (100 mg/kg of body weight) + cDDP (7 mg/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, 100 mg/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.

Pyridine induction of cytochrome P450 1A1, iNOS and metallothionein in Syrian hamsters and protective effects of silymarin.

An in vivo assessment for the protective effects of silymarin for pyridine toxicity was investigated through cytochrome P450 isoform CYP1A1 and inducible nitric oxide synthase (iNOS) activity prevention. Moreover, the effect of pyridine-induced oxidative stress on metallothionein I-II (MT), a scavenger of oxygen-derived free radicals, was investigated. Forty Syrian hamsters were allocated into 4 groups. Syrian hamsters were dosed with pyridine (400mg/kg) intraperitoneally with and without silymarin (200mg/kg daily by gavage) for 4 days. Pyridine induced diffuse degeneration and necrosis of the proximal and distal renal tubular cells; cloudy swelling, necrosis and hepatocellular atypia of the liver; and degenerative changes in the myocardium. The degree of pathological alterations was less severe with simultaneous silymarin application. CYP1A1, iNOS and MT expression levels were elevated in liver, kidney and heart in response to acute pyridine toxicity. Silymarin application abolished or significantly suppressed the induction of CYP1A1, iNOS and MT expressions in liver, kidney and heart of the pyridine-treated Syrian hamsters. Enhanced synthesis of MT by pyridine possibly implies a purposive cellular response to prevent damage caused by oxygen radicals. However, silymarin significantly reduced the oxidative-stress-inducing effect of pyridine as reflected by decreased synthesis of MT. These results suggest that through oxidant generation, pyridine may cause alteration of the metabolic ways, including nitric oxide-mediated CYP1A1 activity.

Royal jelly (honey bee) is a potential antioxidant against cadmium-induced genotoxicity and oxidative stress in albino mice.

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 250 mg/kg of body weight), Cd alone (2 mg/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 250 mg/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.

Protective effect of lycopene against mercury-induced cytotoxicity in albino mice: pathological evaluation.

The present study was carried out to evaluate the protective role of lycopene on cytotoxicity induced by mercury in albino mice. The animals were randomly divided into seven groups. Group I (control) were treated with tap water Group II (positive control) were treated with 20 mg kg(-1) d(-1) lycopene, Group III were treated with 10 mg kg(-1) body weight mercury Group IV were treated with 10 mg kg(-1) body weight mercury + 5 mg kg(-1) d(-1) lycopene, Group V were treated with 10 mg kg(-1) body weight mercury + 10 mg kg(-1) d(-1) lycopene, Group VI were treated with 10 mg kg(-1) body weight mercury + 15 mg kg(-1) d(-1) lycopene, Group VII were treated with 10 mg kg(-1) body weight mercury + 20 mg kg(-1) d(-1) lycopene once a day for 20 consecutive days by oral gavage. The initial and final weights of all mice were measured by sensitive balance in order to investigate the effect of mercury and lycopene on the body weight of mice. Then, MN slides were prepared using the standard MN assay technique with Giemsa staining from erythrocyte cells of each mouse and were scored using binocular light microscope (Japan, Olympus BX 51). The results indicated that, all lycopene-supplemented lymphocytes showed a lower MN frequency than lymphocytes in only mercury-treated group. It was seen that lycopene had protective effect on MN particularly at 20 mg kg(-1) d(-1) dose when compared with the other doses. Besides, weight gain increased depending on dose of applied lycopene when compared with only mercury-treated group. In histopathological examinations, although it has been observed severe changes such as hemorrhage, hepatocyte degeneration and tubular degeneration of kidney in only mercury-treated group, there was an observable regression on the severity and account of these lesions in tissues of mice supplemented with different doses of lycopene. In vivo results showed that the lycopene supplementation decreases cytotoxicity induced by mercury and its protective role is dose-dependent.

Hepatoprotective effect of L-carnitine against acute acetaminophen toxicity in mice.

L-carnitine is a cofactor in the transfer of long-chain fatty acid allowing the beta-oxidation of fatty acid in the mitochondria. It is also a known antioxidant with protective effects against lipid peroxidation. In this study, hepatoprotective effect of L-carnitine was investigated against acetaminophen (AA)-induced liver toxicity where mitochondrial dysfunction and oxidative stress are thought to be involved in AA hepatotoxicity. Sixty-four Balb/C mice were divided into eight groups. Mice were dosed with single-AA injection (500 mg/kg via the intra peritoneal route) with or without L-carnitine (500 mg/kg for 5 days starting 5 days before AA injection via intra peritoneal route) and sampled at 4, 8 and 24 h following AA injection. AA increased serum AST, ALT, total sialic acid (TSA) and MDA as well as tissue TSA and MDA levels significantly with the highest increase observed at 4 h, but there was a decrease in blood and tissue GSH level. Administration of L-carnitine significantly reduced AA-induced elevations in AST, ALT, TSA and MDA concentrations and increased GSH levels at all sampling points. AA also induced necrosis, hyperemia, sinusoidal congestion and hemorrhage with time-dependent increase in severity, but the degree of necrosis and histopathologic alterations were most severe at 24 h following AA administration. However, the degree of pathologic alterations was less severe with simultaneous L-carnitine application. These results suggest that AA results in oxidative damage in the liver with an acute effect. L-carnitine also has a prominent protective effect against AA toxicity and may be of therapeutic value in the treatment of AA-induced hepatotoxicity.