scholarly journals Resveratrol Alleviates Pyraclostrobin Induced Lipid Peroxidation, Oxidative Stress, and DNA Damage in Rats

2021 ◽  
Author(s):  
FAHRIYE ZEMHERI NAVRUZ ◽  
Sinan INCE ◽  
Damla ARSLAN-ACAROZ ◽  
Ulaş ACAROZ ◽  
Hasan Hüseyin DEMIREL ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Protective Effect ◽  
Caspase 3 ◽  
Male Rats ◽  
Histopathological Changes ◽  
Caspase 9 ◽  
Oral Gavage ◽  
Protective Properties ◽  
Expression Levels

Abstract Pyraclostrobin (Pyra) is a fungicide in the strobilurin class and has proven to be very toxic to aquatic species. Resveratrol (Res) is a phytoalexin that exhibits multiple bioactivities as antioxidative, anti-inflammatory, cardiovascular protective, and anti-aging in animals and is found in plant species such as mulberry, peanut, and grape. This study aimed to determine the protective effect of Res against Pyra-induced oxidative stress in rats. For this purpose, a total of 48 male rats divided into 6 groups − 8 in each group - were exposed to 30 mg/kg Pyra by oral gavage once a day for 4 weeks and to 3 different concentrations of Res (5, 10 and 20 mg/kg) together with Pyra. It was observed that, in groups administered with Pyra, malondialdehyde (MDA) levels increased whereas glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels decreased. It was observed that, in the group administered with Pyra, expression levels of CYP2E1 gene, which is associated with increased cancer risk, pro-apoptotic BAX gene, apoptotic caspase-3, caspase-8 and caspase-9 genes, NFκB gene, which is a pro-inflammatory transcription factor, and p53 gene, which plays a regulatory role in the cell, increased whereas expression level of anti-apoptotic bcl-2 gene decreased. It was determined that Res administrations improved Pyra-induced oxidative damage, histopathological changes and expression levels of various genes. According to the ssDNA analysis obtained from the DNA isolated from the blood; when DNA damage and histopathological damage in tissues were examined, it was observed that the highest damage was in the group administered with Pyra and the damage decreased depending on the increase in dose of Res. Consequently, it was observed that Res, known for its antioxidant protective properties, exhibited a protective effect against oxidative stress caused by Pyra.

scholarly journals Efficacy of Melatonin against Oxidative Stress, DNA Damage and Histopathological Changes Induced by Nicotine in Liver and Kidneys of Male Rats

2021 ◽  
Vol 10 (1) ◽  
pp. 31-36
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Histopathological Examination ◽  
Harmful Effect ◽  
Male Rats ◽  
10Mg Dose ◽  
Control Group ◽  
Dna Integrity ◽  
Histopathological Changes ◽  
Antioxidant Parameters

The present study was carried out to investigate and compare the effect of nicotine alone and in combination with melatonin on some oxidants and antioxidant parameters, histopathological changes and DNA integrity in the liver and kidneys of male rats. For this purpose 75 mature male rats weighing 120-140g were randomly divided into five groups; control group (1% ethanol in saline), nicotine group (rats administrated nicotine at a dose of 0.6mg/kg body weight; BW) and nicotine and melatonin groups (rats administrated the same dose of nicotine plus 1, 5 or 10mg/kg BW melatonin, respectively). Nicotine and ‏ melatonin were injected intraperitoneally daily for 21days. Fasting blood samples were collected from each rat one day after the end of last injection (at 22nd day) and sera were collected for determination of total antioxidant capacity (TAC). Five rats were sacrificed from each group; Liver and kidneys were collected for estimation of oxidative stress parameters (MDA, SOD and GSH), histopathological examination and for estimation of DNA damage. The results revealed that nicotine increased MDA, decreased TAC, SOD and GSH, induced histopathological changes and increased the percentage of DNA damage in the liver and kidneys Melatonin administration with nicotine counteracted the effect of nicotine on previous parameters. The effect of melatonin was dose dependent and the 10mg dose produced the highest protective effect. It is concluded that melatonin can ameliorate the harmful effect of nicotine on the liver and kidneys of male rats.

scholarly journals The Protective Effect of Carvacrol on Acetaminophen-Induced Renal Damage in Male Rats

2021 ◽  
Author(s):  
Alireza Najafizadeh ◽  
Ayat Kaeidi ◽  
Mohammadreza Rahmani ◽  
Elham Hakimizadeh ◽  
jalal Hassanshahi
Keyword(s):  
Oxidative Stress ◽  
Serum Creatinine ◽  
Protective Effect ◽  
Renal Damage ◽  
Caspase 3 ◽  
Kidney Tissue ◽  
Group Versus ◽  
Expression Level ◽  
Male Rats ◽  
Sod Activity

Abstract Acetaminophen overdose causes renal injury via oxidative stress and apoptosis induction. Carvacrol has antioxidant effect. The aim of this study was to determine the protective effect of carvacrol on acetaminophen-induced renal damage in male rats. In this experimental study, forty male Wistar rats were randomly divided to five groups (n = 8) including control, carvacrol 10 mg/kg, acetaminophen, acetaminophen + carvacrol 5 mg/kg, and acetaminophen + carvacrol 10 mg/kg. Animals initially received a single dose of acetaminophen (500 mg/kg), then were treated with carvacrol for one week (daily). Afterwards, renal blood flow (RBF), mean arterial pressure (MAP), renal perfusion pressure (RPP), renal vascular resistance (RVR), blood urea nitrogen (BUN), and serum creatinine were measured. Also, malondialdehyde (MDA) concentration, glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity levels were measured in the kidney tissue. Hematoxylin and eosin method was used for histological assessment. The western blotting analysis was used to determine the Bax, Bcl-2 and cleaved caspase-3 proteins expression level in the kidney tissue. Carvacrol (10 mg/kg) could significantly increase the RBF, GPx and SOD activities and also reduced the RVR, serum creatinine, BUN, and MDA in the acetaminophen + carvacrol 10 mg/kg group versus acetaminophen group (P < 0.05). Also, carvacrol significantly decreased the cleaved caspase-3, Bax proteins expression level, and also kidney tissue damage score in the acetaminophen + carvacrol 10 mg/kg group versus acetaminophen group (P < 0.05). This study showed that carvacrol can attenuate the acetaminophen induced acute kidney damage via suppressing oxidative stress, apoptosis and its antioxidant effects.

Anticancer Activity of Platinum (II) Complex with 2-Benzoylpyridine by Induction of DNA Damage, S-Phase Arrest, and Apoptosis

2020 ◽  
Vol 20 (4) ◽  
pp. 504-517
Author(s):  
Yu-Lan Li ◽  
Xin-Li Gan ◽  
Rong-Ping Zhu ◽  
Xuehong Wang ◽  
Duan-Fang Liao ◽  
...  
Keyword(s):  
Dna Damage ◽  
B Cell ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
S Phase ◽  
Caspase 9

Objective: To overcome the disadvantages of cisplatin, numerous platinum (Pt) complexes have been prepared. However, the anticancer activity and mechanism of Pt(II) complexed with 2-benzoylpyridine [Pt(II)- Bpy]: [PtCl2(DMSO)L] (DMSO = dimethyl sulfoxide, L = 2-benzoylpyridine) in cancer cells remain unknown. Methods: Pt(II)-Bpy was synthesized and characterized by spectrum analysis. Its anticancer activity and underlying mechanisms were demonstrated at the cellular, molecular, and in vivo levels. Results: Pt(II)-Bpy inhibited tumor cell growth, especially HepG2 human liver cancer cells, with a halfmaximal inhibitory concentration of 9.8±0.5μM, but with low toxicity in HL-7702 normal liver cells. Pt(II)- Bpy induced DNA damage, which was demonstrated through a marked increase in the expression of cleavedpoly (ADP ribose) polymerase (PARP) and gamma-H2A histone family member X and a decrease in PARP expression. The interaction of Pt(II)-Bpy with DNA at the molecular level was most likely through an intercalation mechanism, which might be evidence of DNA damage. Pt(II)-Bpy initiated cell cycle arrest at the S phase in HepG2 cells. It also caused severe loss of the mitochondrial membrane potential; a decrease in the expression of caspase-9 and caspase-3; an increase in reactive oxygen species levels; the release of cytochrome c and apoptotic protease activation factor; and the activation of caspase-9 and caspase-3 in HepG2 cells, which in turn resulted in apoptosis. Meanwhile, changes in p53 and related proteins were observed including the upregulation of p53, the phosphorylation of p53, p21, B-cell lymphoma-2-associated X protein, and NOXA; and the downregulation of B-cell lymphoma 2. Moreover, Pt(II)-Bpy displayed marked inhibitory effects on tumor growth in the HepG2 nude mouse model. Conclusion: Pt(II)-Bpy is a potential candidate for cancer chemotherapy.

Dexrazoxane does not protect against doxorubicin-induced damage in young rats

2003 ◽  
Vol 285 (2) ◽  
pp. H499-H506 ◽  
Author(s):  
Stéphanie Héon ◽  
Martin Bernier ◽  
Nicolas Servant ◽  
Stevan Dostanic ◽  
Chunlei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Weight Gain ◽  
Heme Oxygenase ◽  
Caspase 3 ◽  
Exercise Program ◽  
Female Rats ◽  
Male Rats ◽  
Heme Oxygenase 1 ◽  
Cardiac Damage

Doxorubicin (DOX), an anticancer drug, causes a dose-dependent cardiotoxicity. Some evidence suggests that female children have an increased risk for DOX-mediated cardiac damage. To determine whether the iron chelator dexrazoxane (DXR) could reduce DOX-induced cardiotoxicity in the young, we injected day 10 neonate female and male rat pups with a single dose of saline or DOX, DXR, or DXR + DOX (20:1). We followed body weight gain with growth, measured cardiac hypertrophy after a 2-wk swim exercise program, markers of apoptosis (Bcl-2, BAX, BNIP1, caspase 3 activation), oxidative stress (heme oxygenase 1, protein carbonyl levels), the chaperone protein clusterin, and the transcriptional activator early growth response gene-1 (Egr-1) in hearts of nonexercised and exercised rats on neonate day 38. All DOX-alone and DXR + DOX-treated rats showed decreased weight gain, with female rats affected earlier than male rats. DXR-alone, DOX-alone, and DXR + DOX-treated rats had an increased heart weight-to-body weight (heart wt/body wt) ratio after the exercise program with female rats showing the largest increase in heart wt/body wt. Drug-treated females also showed increased cardiac apoptosis, as measured by the increased expression of the proapoptotic proteins BAX and BNIP1 and the appearance of caspase 3 activation products, and oxidative stress, as measured by increased heme oxygenase 1 expression, and reduced Egr-1 and clusterin expression when compared with the similarly treated male rats. We conclude that DXR preinjection did not reduce DOX-induced noncardiac and cardiac damage and that young female rats were more susceptible to DXR and DOX toxicities than age-matched male rats.

scholarly journals Protective Effects of Shenfuyixin Granule on H2O2-Induced Apoptosis in Neonatal Rat Cardiomyocytes

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Xinlu Wang ◽  
Xuanxuan Hao ◽  
Youping Wang ◽  
Bin Li ◽  
Lin Cui ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Caspase 3 ◽  
Neonatal Rat ◽  
Caspase 8 ◽  
Caspase 9 ◽  
Rat Cardiomyocytes ◽  
Expression Levels ◽  
Apoptosis Rate ◽  
Neonatal Rat Cardiomyocytes ◽  
Mitochondrion Membrane Potential

Shenfuyixin granule (SFYXG, i.e., Xinshuaikang granule) is a prescription, commonly used in the clinical experience, which plays a significant role in the treatment of heart failure. The purpose of this present research was to investigate the protective effect of SFYXG, and the mechanism about anti-H2O2-induced oxidative stress and apoptosis in the neonatal rat cardiomyocytes. Myocardial cells, as is well known, were divided into 4 groups: normal, model, SFYXG, and coenzyme Q10 group, respectively. Cells viability was determined by MTT assay. Flow cytometry and AO/EB staining were implemented to test the apoptosis rate and intracellular reactive oxygen species (ROS) level. Mitochondrion membrane potential (MMP) was evaluated by JC-1 fluorescence probe method. The myocardial ultrastructure of mitochondrion was measured by electron microscope. The related mRNA expression levels of Bax, Bcl-2, Caspase-3, caspase-8, and caspase-9 were detected by real-time polymerase chain reaction (PCR). Also, the expression levels of Bax and Bcl-2 protein were detected by Western blot, and the expression levels of caspase-3, caspase-8, and caspase-9 protein were tested by caspase-Glo®3 Assay, caspase-Glo®8 Assay, and caspase-Glo®9 Assay, respectively. GAPDH was used as the internal reference gene/protein. The results revealed that SFYXG (0.5 mg/ml) raised the viability of myocardial cell, weakened the apoptosis rate and ROS level, corrected the mitochondrion membrane potential stability, and improved cell morphology and ultrastructure of myocardial mitochondrion. Furthermore, SFYXG upregulated the antiapoptosis gene of Bcl-2, but downregulated the proapoptosis genes of Bax, caspase-3, and caspase-9. In conclusion, SFYXG could appear to attenuate myocardial injury by its antioxidative and antiapoptosis effect.

scholarly journals Potential Protective Effect of Vitamin C on Qunalphos-Induced Cardiac Toxicity: Histological and Tissue Biomarker Assay

Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 39
Author(s):  
Ayed A. Shati ◽  
Mohamed Samir A. Zaki ◽  
Youssef A. Alqahtani ◽  
Mohamed A. Haidara ◽  
Mubarak Al-Shraim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Protective Effect ◽  
Cardiac Tissue ◽  
Electron Microscopic Examination ◽  
Male Rats ◽  
Cardiac Damage ◽  
Electron Microscopic ◽  
Necrosis Factor Alpha ◽  
Vit C

Insecticides and toxicants abound in nature, posing a health risk to humans. Concurrent exposure to many environmental contaminants has been demonstrated to harm myocardial performance and reduce cardiac oxidative stress. The purpose of this research was to study the protective effect of vitamin C (Vit C) on quinalphos (QP)-induced cardiac tissue damage in rats. Eighteen albino male rats were randomly categorised into three groups (n = 6). Control, QP group: rats received distilled water. QP insecticide treatment: an oral administration of QP incorporated in drinking water. QP + Vit C group: rats received QP and Vit C. All the experiments were conducted for ten days. Decline of cardiac antioxidant biomarkers catalase (CAT) and reduced glutathione (GPx) along with increased proinflammatory markers tumour necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) indicated oxidative and inflammatory damage to the heart following administration of QP when compared to control rats. The light microscopic and ultrastructure appearance of QP-treated cardiomyocytes exhibited cardiac damage. Administration of Vit C showed decreased oxidative and inflammatory biomarkers, confirmed with histological and electron microscopic examination. In conclusion, Vit C protected the heart from QP-induced cardiac damage due to decreased inflammation and oxidative stress.

Mitigation of IL-1β, IL-6, TNF-α, and markers of apoptosis by ursolic acid against cisplatin-induced oxidative stress and nephrotoxicity in rats

2021 ◽  
Vol 40 (12_suppl) ◽  
pp. S397-S405
Author(s):  
Pankaj Tripathi ◽  
Saeed Alshahrani
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Uric Acid ◽  
Inflammatory Cytokines ◽  
Caspase 3 ◽  
Caspase 9 ◽  
Histological Damage ◽  
Tnf Α ◽  
Mda Content ◽  
Pro Inflammatory Cytokines

Background: Ursolic acid (UA) is a natural pentacyclic triterpenoid that is known for its benefits under several pathological conditions. Cisplatin (CP) is among the most preferred chemotherapeutic agents; however, its nephrotoxicity limits its clinical utility. Purpose: This study was aimed to determine the role of UA in the reduction of CP-induced nephrotoxicity and mitigation of pro-inflammatory cytokines and apoptosis in a rat model. Methodology: Male Wistar rats were randomized into vehicle control, CP (7.5 mg/kg), UA 10 mg/kg, and CP with UA 5 and 10 mg/kg groups. Kidney and blood samples were collected for assessment of renal function, measurement of pro-inflammatory cytokines, apoptosis markers, antioxidant activity, and tissue histology. Results: CP significantly increased the levels of serum Cr, BUN, and uric acid; it also induced histological damage reflecting the pathophysiology observed during nephrotoxicity. CP has also shown its pro-oxidant activity in kidney tissue because CP decreased the levels of GSH, SOD, and CAT; it increased the lipid peroxidation as measured by MDA content. In addition, CP significantly upregulated the activity of pro-inflammatory cytokines and expression of apoptotic markers, that is, there were increased levels of IL-1β, IL-6, TNF-α, caspase-3, and caspase-9. Two weeks of continuous treatment of UA showed significant recovery against CP-induced nephrotoxicity; UA decreased the levels of Cr, BUN, and uric acid and ameliorated histological damage. UA also downregulated the activities of IL-1β, IL-6, and TNF-α as well as expression of caspase-3 and caspase-9. Furthermore, CP-induced oxidative stress that was antagonized by UA—the levels of GSH, SOD, and CAT were significantly increased while MDA content was decreased. Conclusions: UA has a protective effect against CP-induced nephrotoxicity, which may be due to its antioxidant activity and mitigation of ILβ-1, ILβ-6, TNF-α, and markers of apoptosis.

DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3

Development ◽  
2001 ◽  
Vol 128 (1) ◽  
pp. 137-146
Author(s):  
C. D'Sa-Eipper ◽  
J.R. Leonard ◽  
G. Putcha ◽  
T.S. Zheng ◽  
R.A. Flavell ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cell Apoptosis ◽  
Neuronal Apoptosis ◽  
Caspase 3 ◽  
Precursor Cell ◽  
Neural Precursor ◽  
Normal Brain ◽  
Neural Precursor Cell ◽  
Caspase 9

Programmed cell death (apoptosis) is critical for normal brain morphogenesis and may be triggered by neurotrophic factor deprivation or irreparable DNA damage. Members of the Bcl2 and caspase families regulate neuronal responsiveness to trophic factor withdrawal; however, their involvement in DNA damage-induced neuronal apoptosis is less clear. To define the molecular pathway regulating DNA damage-induced neural precursor cell apoptosis, we have examined the effects of drug and gamma-irradiation-induced DNA damage on telencephalic neural precursor cells derived from wild-type embryos and mice with targeted disruptions of apoptosis-associated genes. We found that DNA damage-induced neural precursor cell apoptosis, both in vitro and in vivo, was critically dependent on p53 and caspase 9, but neither Bax nor caspase 3 expression. Neural precursor cell apoptosis was also unaffected by targeted disruptions of Bclx and Bcl2, and unlike neurotrophic factor-deprivation-induced neuronal apoptosis, was not associated with a detectable loss of cytochrome c from mitochondria. The apoptotic pathway regulating DNA damage-induced neural precursor cell death is different from that required for normal brain morphogenesis, which involves both caspase 9 and caspase 3 but not p53, indicating that additional apoptotic stimuli regulate neural precursor cell numbers during telencephalic development.

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