scholarly journals Mitigating Potentials of Antioxidant-Rich Plants in Earthworms Exposed to Glyphosate

2021 ◽  
Author(s):  
Isaac O Ayanda ◽  
Tolulope O. Ajayi
Keyword(s):  
Dna Damage ◽  
Eisenia Fetida ◽  
Control Group ◽  
Soil Organisms ◽  
Antioxidant Responses ◽  
Ocimum Gratissimum ◽  
Telfairia Occidentalis ◽  
Enzyme Superoxide Dismutase ◽  
High Concentrations ◽  
Significant Mortality

Abstract Glyphosate is a non-selective herbicide that has adverse effects on non-target organisms. This present study investigated the toxic effects of glyphosate on earthworms and the potential of antioxidant-rich plants, Ocimum gratissimum and Telfairia occidentalis remediate these effects. Earthworms (Eisenia fetida) were placed into four groups and treated with concentrations of 1, 2 and 3% glyphosate in soil. The last group was a control group. The worms were collected on the 3rd, 7th and 14th, days post-exposure. During these intervals, the weight of the worms and activities of antioxidant enzyme - superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), malondialdehyde (MDA) were measured to determine the level of antioxidant responses. Furthermore, the percentage of DNA fragmentation was measured to assess the level of DNA damage. Compared with the control group, earthworms exposed to glyphosate and fed with Ocimum gratissimum and Telfairia occidentalis showed varying responses, with increased activities of CAT, SOD, GSH and reduced levels of MDA. Also, decreased fragmented DNA was observed in earthworm groups fed with Ocimum gratissimum and Telfairia occidentalis in comparison with the group treated exclusively with the herbicide. These results suggest that toxicity from glyphosate exposure significantly reduced oxidative damage, lipid peroxidation and DNA damage in Eisenia fetida by the antioxidant-rich plants. It is conceivable that soil organisms could suffer a significant mortality when exposed to high concentrations of glyphosate. The cultivation of these plants should be encouraged while caution should be exercised in the use of the herbicides.

The Toxicity of Castor Beans and its Treatment with Doxycycline in Local Rabbits

2018 ◽  
Vol 9 (2) ◽  
Author(s):  
Nael Mohammed Sarheed ◽  
Osamah Faisal Kokas ◽  
Doaa Abd Alabas Muhammed Ridh
Keyword(s):  
Castor Bean ◽  
The Body ◽  
Control Group ◽  
High Concentration ◽  
Biochemical Tests ◽  
Doxycycline Treatment ◽  
High Concentrations ◽  
Physiological Tests ◽  
Animal House ◽  
Physiological And Biochemical

The plant of castor is widely spread in the Iraqi land, and characterized with containing ricin toxin, which has a very serious effects, and because the seeds of this plant scattered in the agricultural soil and rivers water, which increases the exposure of humans and animals to these beans. Objective: This experiment was designed to study the effect of high concentration of castor bean powder in some physiological and biochemical parameters and changes in some tissues of the body, as well as trying to use doxycycline to reduce the effects of ingestion of these seeds. Materials and Methods: In the experiment, 24 local rabbits were raised and fed in the Animal House of the Faculty of Medicine / Al-Muthanna University, then divided into four groups and treated for three weeks (21 days), Control group: treated with normal saline solution (0.9) orally throughout the experiment, G1: was treated orally with a concentration of 25 mg / kg of castor bean powder daily during the experiment, G2 : orally treated 25 mg / kg of castor bean and 25 mg / kg of doxycycline, G3: orally treated 25 mg / kg of castor powder with 50 mg / kg of doxycycline daily throughout the trial period. Results: The results of the experiment showed significant changes (P less than 0.05) in all physiological and biochemical blood tests when compared with control group. There was a significant decrease in PCV, Hb, RBC, T.protein and body weights, while demonstrated a significant increase in WBC, Urea, Creatinine, ALT, AST and ALP, with distortions in liver and kidney of animals that treated with Castor beans. In contrast, the treatment with doxycycline and caster beans showed significant improvement reflected by a normal proportion in physiological tests and biochemical tests with improvement in the tissues when compared to control group. Conclusions: It can be concluded from this study that castor bean has high toxic and pathogenic effects that may be dangerous to the life of the organism. Therefore, it is advisable to be cautious of these pills and avoid exposure to them, also recommended to take high concentrations of doxycycline treatment when infected with castor bean poisoning.

Assessment of oxidative DNA damage, oxidative stress responses and histopathological alterations in gill and liver tissues of Oncorhynchus mykiss treated with linuron

2020 ◽  
pp. 096032712098420
Author(s):  
Ahmet Topal ◽  
Arzu Gergit ◽  
Mustafa Özkaraca
Keyword(s):  
Dna Damage ◽  
Stress Responses ◽  
Oxidative Dna Damage ◽  
Chloride Cells ◽  
Histopathological Changes ◽  
Sod Activity ◽  
Antioxidant Responses ◽  
Secondary Lamellae ◽  
Antioxidant Parameters ◽  
Oxidative Stress Responses

We investigated changes in 8-hydroxy-2-deoxyguanosine (8-OHdG) activity which is a product of oxidative DNA damage, histopathological changes and antioxidant responses in liver and gill tissues of rainbow trout, following a 21-day exposure to three different concentrations of linuron (30 µg/L, 120 µg/L and 240 µg/L). Our results indicated that linuron concentrations caused an increase in LPO levels of liver and gill tissues ( p < 0.05). While linuron induced both increases and decreases in GSH levels and SOD activity, CAT activity was decreased by all concentrations of linuron ( p < 0.05). The immunopositivity of 8-OHdG was detected in the hepatocytes of liver and in the epithelial and chloride cells of the secondary lamellae of the gill tissues. Our results suggested that linuron could cause oxidative DNA damage by causing an increase in 8-OHdG activity in tissues, and it induces histopathological damage and alterations in the antioxidant parameters of the tissues.

scholarly journals Genotoxic and oxidative effect of duloxetine on mouse brain and liver tissues

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Isela Álvarez-González ◽  
Scarlett Camacho-Cantera ◽  
Patricia Gómez-González ◽  
Michael J. Rendón Barrón ◽  
José A. Morales-González ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Damage ◽  
Mouse Brain ◽  
Control Level ◽  
Dna Oxidation ◽  
Methyl Methanesulfonate ◽  
Control Group ◽  
Oxidative Potential ◽  
The Brain ◽  
Oxidative Effect

AbstractWe evaluated the duloxetine DNA damaging capacity utilizing the comet assay applied to mouse brain and liver cells, as well as its DNA, lipid, protein, and nitric oxide oxidative potential in the same cells. A kinetic time/dose strategy showed the effect of 2, 20, and 200 mg/kg of the drug administered intraperitoneally once in comparison with a control and a methyl methanesulfonate group. Each parameter was evaluated at 3, 9, 15, and 21 h postadministration in five mice per group, except for the DNA oxidation that was examined only at 9 h postadministration. Results showed a significant DNA damage mainly at 9 h postexposure in both organs. In the brain, with 20 and 200 mg/kg we found 50 and 80% increase over the control group (p ≤ 0.05), in the liver, the increase of 2, 20, and 200 mg/kg of duloxetine was 50, 80, and 135% in comparison with the control level (p ≤ 0.05). DNA, lipid, protein and nitric oxide oxidation increase was also observed in both organs. Our data established the DNA damaging capacity of duloxetine even with a dose from the therapeutic range (2 mg/kg), and suggest that this effect can be related with its oxidative potential.

scholarly journals Glycyrrhizin Attenuates Carcinogenesis by Inhibiting the Inflammatory Response in a Murine Model of Colorectal Cancer

2021 ◽  
Vol 22 (5) ◽  
pp. 2609
Author(s):  
Guifeng Wang ◽  
Keiichi Hiramoto ◽  
Ning Ma ◽  
Nobuji Yoshikawa ◽  
Shiho Ohnishi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Dna Damage ◽  
Stem Cell ◽  
Inflammatory Response ◽  
Murine Model ◽  
Licorice Root ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Stem Cell Markers ◽  
Tnf Α

Glycyrrhizin (GL), an important active ingredient of licorice root, which weakens the proinflammatory effects of high-mobility group box 1 (HMGB1) by blocking HMGB1 signaling. In this study, we investigated whether GL could suppress inflammation and carcinogenesis in an azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced murine model of colorectal cancer. ICR mice were divided into four groups (n = 5, each)—control group, GL group, colon cancer (CC) group, and GL-treated CC (CC + GL) group, and sacrificed after 20 weeks. Plasma levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α were measured using an enzyme-linked immunosorbent assay. The colonic tissue samples were immunohistochemically stained with DNA damage markers (8-nitroguanine and 8-oxo-7,8-dihydro-2′-deoxy-guanosine), inflammatory markers (COX-2 and HMGB1), and stem cell markers (YAP1 and SOX9). The average number of colonic tumors and the levels of IL-6 and TNF-α in the CC + GL group were significantly lower than those in the CC group. The levels of all inflammatory and cancer markers were significantly reduced in the CC + GL group. These results suggest that GL inhibits the inflammatory response by binding HMGB1, thereby inhibiting DNA damage and cancer stem cell proliferation and dedifferentiation. In conclusion, GL significantly attenuates the pathogenesis of AOM/DSS-induced colorectal cancer by inhibiting HMGB1-TLR4-NF-κB signaling.

scholarly journals Protection of sperm DNA against oxidative stress in vivo by accessory sex gland secretions in male hamsters

Reproduction ◽  
2002 ◽  
pp. 491-499 ◽  
Author(s):  
H Chen ◽  
MP Cheung ◽  
PH Chow ◽  
AL Cheung ◽  
W Liu ◽  
...  
Keyword(s):  
Dna Damage ◽  
Comet Assay ◽  
Prostate Gland ◽  
Single Strand ◽  
Ventral Prostate ◽  
Control Group ◽  
Dna Breakage ◽  
Accessory Glands ◽  
Sperm Dna ◽  
Epididymal Spermatozoa

Reactive oxygen species scavengers present in male accessory sex gland secretions might afford antioxidant protection to sperm DNA. This study was conducted to determine whether accessory sex gland secretions protect the genome and function of spermatozoa against oxidative damage in the uterus. Male golden hamsters were divided into four experimental groups: (i) all accessory sex glands removed; (ii) ampullary glands removed; (iii) ventral prostate gland removed and (iv) sham-operated controls. Ejaculated spermatozoa recovered from uteri 15-30 min after mating with experimental males and caput and cauda epididymal spermatozoa obtained from intact males were incubated in 0-20 mmol NADPH l(-1) for 2 h. These spermatozoa and untreated uterine spermatozoa were processed for two types of comet assay (single cell gel electrophoresis): alkaline comet assay (pH > 13) which revealed single-strand DNA breakage and neutral comet assay (pH 9) which revealed double-strand DNA breakage. In comparison with the sham-operated controls, spermatozoa that had not been exposed to accessory sex gland secretions had a higher incidence and more extensive single-strand DNA damage with increasing concentrations of NADPH. Spermatozoa from hamsters without ampullary glands and from hamsters without the ventral prostate glands were similar to those of the control group. After incubation with NADPH, the capacity of spermatozoa from hamsters without accessory glands and from sham-operated controls to fuse with oocytes in vitro was reduced. However, only hamsters without accessory glands showed a negative correlation between single-strand DNA damage and sperm-oocyte fusion. Cauda epididymal spermatozoa were less susceptible to NADPH treatment compared with caput epididymal spermatozoa. The results of the present study showed that male accessory sex gland secretions can preserve the integrity of the sperm genome.

Oxidative stress and DNA damage induced by trifloxystrobin on earthworms (Eisenia fetida) in two soils

2021 ◽  
pp. 149004
Author(s):  
Ruolin Wu ◽  
Tongtong Zhou ◽  
Jun Wang ◽  
Jinhua Wang ◽  
Zhongkun Du ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Eisenia Fetida

scholarly journals DNA damage in acute myeloid leukemia patients of Northern Mexico

2017 ◽  
Author(s):  
Martha I. Dávila-Rodríguez ◽  
Elva I. Cortés-Gutiérrez ◽  
Roberto Hernández-Valdés ◽  
Karla Guzmán-Cortés ◽  
Rosa E. De León-Cantú ◽  
...  
Keyword(s):  
Dna Damage ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Fluorescent In Situ Hybridization ◽  
Control Group ◽  
Repair Pathway ◽  
Blood Leukocytes ◽  
Northern Mexico ◽  
Acute Myeloid

The purpose of this study was to evaluate DNA damage in the whole genome of peripheral blood leukocytes from patients with acute myeloid leukemia (AML) compared with a control group using DNA breakage detection-fluorescent in situ hybridization (DBD-FISH). Our results suggest that the DNA damage detected in patients with newly diagnosed AML was similar to that observed for the controls; this might be explained by the stimulation of a repair pathway by the pathogenesis itself. These findings indicate that inhibiting the repair pathway could be proposed to enhance the efficacy of chemotherapy.

scholarly journals Persistent Increased Frequency of Genomic Instability in Women Diagnosed with Breast Cancer: Before, during, and after Treatments

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Márcia Fernanda Correia Jardim Paz ◽  
André Luiz Pinho Sobral ◽  
Jaqueline Nascimento Picada ◽  
Ivana Grivicich ◽  
Antonio Luiz Gomes Júnior ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Comet Assay ◽  
Peripheral Blood ◽  
Micronucleus Test ◽  
Cancer Control ◽  
Control Group ◽  
Breast Cancer Patients ◽  
Buccal Cells ◽  
Oncological Treatment

This study aimed to evaluate DNA damage in patients with breast cancer before treatment (background) and after chemotherapy (QT) and radiotherapy (RT) treatment using the Comet assay in peripheral blood and the micronucleus test in buccal cells. We also evaluated repair of DNA damage after the end of RT, as well as the response of patient’s cells before treatment with an oxidizing agent (H2O2; challenge assay). Fifty women with a mammographic diagnosis negative for cancer (control group) and 100 women with a diagnosis of breast cancer (followed up during the treatment) were involved in this study. The significant DNA damage was observed by increasing in the index and frequency of damage along with the increasing of the frequency of micronuclei in peripheral blood and cells of the buccal mucosa, respectively. Despite the variability of the responses of breast cancer patients, the individuals presented lesions on the DNA, detected by the Comet assay and micronucleus Test, from the diagnosis until the end of the oncological treatment and were more susceptible to oxidative stress. We can conclude that the damages were due to clastogenic and/or aneugenic effects related to the neoplasia itself and that they increased, especially after RT.

scholarly journals Sulforaphane-Mediated Nrf2 Activation Prevents Radiation-Induced Skin Injury through Inhibiting the Oxidative-Stress-Activated DNA Damage and NLRP3 Inflammasome

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1850
Author(s):  
Jinlong Wei ◽  
Qin Zhao ◽  
Yuyu Zhang ◽  
Weiyan Shi ◽  
Huanhuan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Western Blotting ◽  
Nlrp3 Inflammasome ◽  
Fibrous Tissue ◽  
Mouse Skin ◽  
Control Group ◽  
Skin Injury ◽  
Antioxidant Genes ◽  
Radiation Induced

This article mainly observed the protective effect of sulforaphane (SFN) on radiation-induced skin injury (RISI). In addition, we will discuss the mechanism of SFN’s protection on RISI. The RISI model was established by the irradiation of the left thigh under intravenous anesthesia. Thirty-two C57/BL6 mice were randomly divided into control group (CON), SFN group, irradiation (IR) group, and IR plus SFN (IR/SFN) group. At eight weeks after irradiation, the morphological changes of mouse skin tissues were detected by H&E staining. Then, the oxidative stress and inflammatory response indexes in mouse skin tissues, as well as the expression of Nrf2 and its downstream antioxidant genes, were evaluated by ELISA, real-time PCR, and Western blotting. The H&E staining showed the hyperplasia of fibrous tissue in the mouse dermis and hypodermis of the IR group. Western blotting and ELISA results showed that the inflammasome of NLRP3, caspase-1, and IL-1β, as well as oxidative stress damage indicators ROS, 4-HNE, and 3-NT, in the skin tissues of mice in the IR group were significantly higher than those in the control group (p < 0.05). However, the above pathological changes declined sharply after SFN treatment (p < 0.05). In addition, the expressions of Nrf2 and its regulated antioxidant enzymes, including CAT and HO-1, were higher in the skin tissues of SFN and IR/SFN groups, but lower in the control and IR groups (p < 0.05). SFN may be able to suppress the oxidative stress by upregulating the expression and function of Nrf2, and subsequently inhibiting the activation of NLRP3 inflammasome and DNA damage, so as to prevent and alleviate the RISI.

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