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.
The current study was undertaken to assess the attenuating potential of lycopene against Dithane toxicity in Alliumcepa 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.
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 (NiCl
2
)-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 NiCI
2
, 1 mg/L NiCI
2
+ 440 mg/L turmeric, and 1 mg/L NiCI
2
+ 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. NiCl
2
reduced germination percentage, root elongation, and weight gain. Following NiCl
2
application, the frequency of aberrant chromosomes and micronuclei increased, while mitotic index decreased. NiCl
2
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 NiCl
2
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 NiCl
2
. Data from the study suggests that turmeric has remarkable protection potential against NiCl
2
in
Allium cepa
.
The toxic effects of methiocarb insecticide were investigated using bulbs of Allium cepa as test material. Physiological effects were investigated with rooting percentage, root length, and weight ...gain; Cytogenetic effects were analyzed with micronucleus (MN), chromosomal damage and mitotic index (MI) and anatomical effects were investigated on root tip cell. Biochemical effects were investigated by measuring the malondialdehyde (MDA) levels, catalase (CAT) and superoxide dismutase (SOD) activities. For this aim, A. cepa bulbs were divided into four groups, one control, and three applications; the bulbs in the control group were treated with tap water; the bulbs in the application group were treated with 2.5 mg L−1, 5.0 mg L−1 and 7.5 mg L−1 doses of methiocarb for 72 h. Methiocarb administration caused a decrease in physiological parameters compared to the control group. Methiocarb administration caused an increase in the number of MN and chromosomal damage, and a decrease in MI, besides methiocarb application caused some anatomical damages on cells of root tips. Methiocarb administration caused a dose-dependent increase in CAT and SOD activities and MDA levels compared to the control group. As a result, methiocarb caused toxic effects, and the Allium test material was found to be a useful bioindicator for monitoring these effects.
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.
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.
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.
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.
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.
•H2S is an important mediator that regulates vascular tone including ocular arteries.•NaHS dilates retinal artery mainly via activation of myosin phosphatase.•H2S might have a therapeutic value in some ocular diseases.
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.
In this study, the protective effects of Ginkgo biloba leaf extract (GbE) against toxicity induced by hydrogen peroxide (H
2
O
2
) 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 H
2
O
2
for 45 consecutive days. It was observed that H
2
O
2
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 H
2
O
2
, 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 H
2
O
2
and reduces the MN and CAs frequency and causes a re-increase in mitotic cell numbers. It was determined that H
2
O
2
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 H
2
O
2
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 H
2
O
2
.
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.
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