No abstract

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 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 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.

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.

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.

No abstract

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.