scholarly journals Manganese-Induced Nephrotoxicity Is Mediated through Oxidative Stress and Mitochondrial Impairment

2020 ◽  
Vol 4 (2) ◽  
pp. 1-10 ◽  
Author(s):  
Amir Mohammad Niknahad ◽  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Leila Moezi ◽  
Reza Heidari
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Essential Element ◽  
The Other ◽  
Tubular Atrophy ◽  
Mitochondrial Impairment ◽  
Other Hand ◽  
Markers Of Oxidative Stress ◽  
Dehydrogenases Activity

Manganese (Mn) is an essential element that is incorporated in various metabolic pathways and enzyme structures. On the other hand, a range of adverse effects has been described in association with Mn overexposure. Mn is a well-known neurotoxic agent in mammals. Renal injury is another adverse effect associated with Mn intoxication. No precise mechanism for Mn nephrotoxicity has been identified so far. The current study was designed to evaluate the potential mechanisms of Mn-induced renal injury. Rats were treated with Mn (20 and 40 mg/mL, respectively, in drinking water) for 30 consecutive days. Markers of oxidative stress, as well as several mitochondrial indices, were assessed in the kidney tissue. Renal injury was evident in Mn-treated animals, as judged by a significant increase in serum BUN and creatinine. Moreover, urinalysis revealed a significant increase in urine glucose, phosphate, and protein in Mn-treated rats. Kidney histopathological alterations, including tubular atrophy, interstitial inflammation, and necrosis, were also detected in Mn-treated animals. Biomarkers of oxidative stress, including an increment in reactive oxygen species (ROS), lipid peroxidation, and oxidized glutathione (GSSG), were detected in Mn-treated groups. On the other hand, kidney glutathione (GSH) stores and total antioxidant capacity were depleted in Mn groups. Mn exposure was associated with significant mitochondrial depolarization, decreased mitochondrial dehydrogenases activity, mitochondrial permeabilization, and depletion of adenosine tri-phosphate (ATP) content. These data highlight oxidative stress and mitochondrial impairment as potential mechanisms involved in Mn-induced renal injury.

scholarly journals The Role of Mitochondrial Impairment and Oxidative Stress in the Pathogenesis of Lithium-Induced Reproductive Toxicity in Male Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohammad Mehdi Ommati ◽  
Mohammad Reza Arabnezhad ◽  
Omid Farshad ◽  
Akram Jamshidzadeh ◽  
Hossein Niknahad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adverse Effects ◽  
Reproductive Toxicity ◽  
The Other ◽  
Mitochondrial Depolarization ◽  
Mitochondrial Impairment ◽  
Other Hand ◽  
Wide Range ◽  
The Impact ◽  
Testis Tissue

Lithium (Li+) is prescribed against a wide range of neurological disorders. Besides its excellent therapeutic properties, there are several adverse effects associated with Li+. The impact of Li+ on renal function and diabetes insipidus is the most common adverse effect of this drug. On the other hand, infertility and decreased libido is another complication associated with Li+. It has been found that sperm indices of functionality, as well as libido, is significantly reduced in Li+-treated men. These adverse effects might lead to drug incompliance and the cessation of drug therapy. Hence, the main aims of the current study were to illustrate the mechanisms of adverse effects of Li+ on the testis tissue, spermatogenesis process, and hormonal changes in two experimental models. In the in vitro experiments, Leydig cells (LCs) were isolated from healthy mice, cultured, and exposed to increasing concentrations of Li+ (0, 10, 50, and 100 ppm). In the in vivo section of the current study, mice were treated with Li+ (0, 10, 50, and 100 ppm, in drinking water) for five consecutive weeks. Testis and sperm samples were collected and assessed. A significant sign of cytotoxicity (LDH release and MTT assay), along with disrupted testosterone biosynthesis, impaired mitochondrial indices (ATP level and mitochondrial depolarization), and increased biomarkers of oxidative stress were detected in LCs exposed to Li+. On the other hand, a significant increase in serum and testis Li+ levels were detected in drug-treated mice. Moreover, ROS formation, LPO, protein carbonylation, and increased oxidized glutathione (GSSG) were detected in both testis tissue and sperm specimens of Li+-treated mice. Several sperm anomalies were also detected in Li+-treated animals. On the other hand, sperm mitochondrial indices (mitochondrial dehydrogenases activity and ATP levels) were significantly decreased in drug-treated groups where mitochondrial depolarization was increased dose-dependently. Altogether, these data mention oxidative stress and mitochondrial impairment as pivotal mechanisms involved in Li+-induced reproductive toxicity. Therefore, based on our previous publications in this area, therapeutic options, including compounds with high antioxidant properties that target these points might find a clinical value in ameliorating Li+-induced adverse effects on the male reproductive system.

Beneficial effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin in rats

2015 ◽  
Vol 35 (3) ◽  
pp. 276-281 ◽  
Author(s):  
H Elbe ◽  
Z Dogan ◽  
E Taslidere ◽  
A Cetin ◽  
Y Turkoz
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Histopathological Changes ◽  
Tubular Atrophy ◽  
Beneficial Effects ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

Ciprofloxacin is a broad-spectrum quinolone antibiotic commonly used in clinical practice. Quercetin is an antioxidant belongs to flavonoid group. It inhibits the production of superoxide anion. In this study, we aimed to evaluate the effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin. Twenty-eight female Wistar albino rats were divided into four groups: control, quercetin (20 mg kg−1 day−1 gavage for 21 days), ciprofloxacin (20 mg kg−1 twice a day intraperitoneally for 10 days), and ciprofloxacin + quercetin. Samples were processed for histological and biochemical evaluations. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), and catalase (CAT) activities were measured in kidney tissue. The ciprofloxacin group showed histopathological changes such as infiltration, dilatation in tubules, tubular atrophy, reduction of Bowman’s space, congestion, hemorrhage, and necrosis. In the ciprofloxacin + quercetin group, these histopathological changes markedly reduced. MDA levels increased in the ciprofloxacin group and decreased in the ciptofloxacin + quercetin group. SOD and CAT activities and GSH levels significantly decreased in the ciprofloxacin group. On the other hand, in the ciprofloxacin + quercetin group, SOD and CAT activities and GSH levels significantly increased with regard to the ciprofloxacin group. We concluded that quercetin has antioxidative and therapeutic effects on renal injury and oxidative stress caused by ciprofloxacin in rats.

The ethanol leaf extract of Andrographis paniculata blunts acute renal failure in cisplatin-induced injury in rats through inhibition of Kim-1 and upregulation of Nrf2 pathway

2018 ◽  
Vol 30 (2) ◽  
pp. 205-217 ◽  
Author(s):  
Bisi O. Adeoye ◽  
Ademola A. Oyagbemi ◽  
Ebunoluwa R. Asenuga ◽  
Temidayo O. Omobowale ◽  
Adeolu A. Adedapo
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Serum Creatinine ◽  
Leaf Extract ◽  
Histopathological Examination ◽  
Hematological Parameters ◽  
Kidney Tissue ◽  
Inflammatory Cells ◽  
Andrographis Paniculata ◽  
Markers Of Oxidative Stress

Abstract Background Cisplatin (CP) is a novel drug of choice in the treatment of cancer but its major limitation is nephrotoxicity, which is dose limiting. Andrographis paniculata (AP) is a common Indian dietary component. It is well known for its medicinal properties. This present study investigated the nephroprotective effect of ethanol leaf extract of Andrographis paniculata (EEAP) on CP-induced nephrotoxicity. Methods CP was used to induce nephrotoxicity in male Wistar rats to study the effect of EEAP on renal damages using hematological parameters, biochemical parameters, histology, and immunohistochemistry studies. Results The effects of EEAP were determined by CP-induced changes in different kidney tissue on antioxidant enzymes, markers of oxidative stress, serum creatinine, and urine parameters. Administration of EEAP (200 mL/kg and 400 mg/kg orally), prior to and following a single dose CP treatment (10 mg/kg i.p), significantly mitigated the CP-induced decrease in antioxidant enzymes, and increase in markers of oxidative stress, serum creatinine, and urinary protein. On histopathological examination of the kidney tissue, there was severe glomerular degeneration and infiltration of inflammatory cells in CP only treated rats, mild glomerular degeneration, and infiltration of inflammatory cells in EEAP pre-treated rats. Furthermore, EEAP activated Nrf2 and mitigated Kim-1 pathways in CP-induced nephrotoxicity. Conclusions The results showed the protective effect of EEAP against CP-induced nephrotoxicity.

scholarly journals Lycopene supplementation prevents reactive oxygen species mediated apoptosis in Sertoli cells of adult albino rats exposed to polychlorinated biphenyls

2013 ◽  
Vol 6 (2) ◽  
pp. 83-92 ◽  
Author(s):  
Gunasekaran Krishnamoorthy ◽  
Kandaswamy Selvakumar ◽  
Prabhu Venkataraman ◽  
Perumal Elumalai ◽  
Jagadeesan Arunakaran
Keyword(s):  
Oxidative Stress ◽  
Polychlorinated Biphenyls ◽  
Sertoli Cell ◽  
Sertoli Cells ◽  
Caspase 3 ◽  
Sperm Count ◽  
Reactive Oxygen ◽  
The Other ◽  
Sperm Production ◽  
Other Hand

Abstract Sertoli cell proliferation is attenuated before attaining puberty and the number is fixed in adult testes. Sertoli cells determine both testis size and daily sperm production by providing physical and metabolic support to spermatogenic cells. Polychlorinated biphenyls (PCBs) exposure disrupts functions of Sertoli cells causing infertility with decreased sperm count. On the other hand, lycopene is improving sperm count and motility by reducing oxidative stress in humans and animals. Hence we hypothesized that PCBs-induced infertility might be due to Sertoli cell apoptosis mediated by oxidative stress and lycopene might prevent PCBs-induced apoptosis by acting against oxidative stress. To test this hypothesis, animals were treated with vehicle control, lycopene, PCBs and PCBs + lycopene for 30 days. After the experimental period, the testes and cauda epididymidis were removed for isolation of Sertoli cells and sperm, respectively. We observed increased levels of oxidative stress markers (H2O2 and LPO) levels, increased expression of apoptotic molecules (caspase-8, Bad, Bid, Bax, cytochrome C and caspase-3), decreased anti-apoptotic (Bcl2) molecule and elevated apoptotic marker activity (caspase-3) in Sertoli cells of PCBs-exposed animals. These results were associated with decreased sperm count and motility in PCBs exposed animals. On the other hand, lycopene prevented the elevation of Sertoli cellular apoptotic parameters and prevented the reduction of sperm parameters (count and motility). The data confirmed that lycopene as an antioxidant scavenged reactive oxygen substances, prevented apoptosis, maintained normal function in Sertoli cells and helped to provide physical and metabolic support for sperm production, thereby treating infertility in men.

scholarly journals Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox?

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Subrata Kumar Biswas
Keyword(s):  
Oxidative Stress ◽  
Chronic Diseases ◽  
Inflammatory Process ◽  
The Other ◽  
Present Review ◽  
Low Grade ◽  
Inflammatory Pathways ◽  
Pathological Conditions ◽  
Other Hand ◽  
And Oxidative Stress

Oxidative stress has been implicated in many chronic diseases. However, antioxidant trials are so far largely unsuccessful as a preventive or curative measure. Chronic low-grade inflammatory process, on the other hand, plays a central role in the pathogenesis of a number of chronic diseases. Oxidative stress and inflammation are closely related pathophysiological processes, one of which can be easily induced by another. Thus, both processes are simultaneously found in many pathological conditions. Therefore, the failure of antioxidant trials might result from failure to select appropriate agents that specifically target both inflammation and oxidative stress or failure to use both antioxidants and anti-inflammatory agents simultaneously or use of nonselective agents that block some of the oxidative and/or inflammatory pathways but exaggerate the others. To examine whether the interdependence between oxidative stress and inflammation can explain the antioxidant paradox we discussed in the present review the basic aspects of oxidative stress and inflammation and their relationship and dependence.

scholarly journals Effects of aerobic training on oxidative stress and inflammation in rats exposed to controlled emissions of carbon monoxide (CO) and nitrogen dioxide (NO2)

2020 ◽  
Vol 8 (2) ◽  
pp. 099-110
Author(s):  
Tito S. Albérick I ◽  
Nsompi Florent ◽  
Messan Folly ◽  
Kpatcha Tchazou ◽  
Lawani M. Mansourou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Monoxide ◽  
Nitrogen Dioxide ◽  
Aerobic Exercise ◽  
Ambient Air ◽  
Repeated Exposure ◽  
The Other ◽  
Training Block ◽  
Other Hand ◽  
Tnf Α

The objective of this study is to determine the effects of isolated exercise and those of repeated exercise on oxidative stress and the inflammatory process following exposure to carbon monoxide (CO) and nitrogen dioxide (NO2). Material and Method: 15 male Wistar rats, all eight weeks old, were randomly assigned to three groups. CO and NO2 were produced by the combustion of diesel fuel using a device contained in a sealed metal box and supplied with ambient air by a pump. The ranges of CO and NO2 concentrations to which the rats were exposed ranged from 35 to 45 ppm and 0.2 to 0.3 ppm, respectively. The aerobic workouts were performed on a rat treadmill. Blood samples were taken 24 hours after completion of handling at D4, D9 and D14. Variables studied were Malondialdehyde (MDA) and Tumor Necrosis Factor-alpha (TNF-α). Results: Aerobic endurance training after repeated exposure to CO and NO2 induces at the end of the first training block (D4) a significant increase (p ˂ 0.01) in MDA and TNF-α. On the other hand, the second block (D9) and the third training block (D14) induced a significant decrease (p ˂ 0.01) in these same parameters. Conclusion: Aerobic exercise practiced in isolation exacerbates the oxidative stress and inflammation induced by exposure to CO and NO2. On the other hand, regular aerobic exercise in a less polluted environment, following five days of recovery, significantly reduces the high levels of oxidative stress and inflammation caused by repeated exposure to automobile pollutants.

scholarly journals Upregulation of Peroxiredoxin 3 Protects Afg3l2-KO Cortical Neurons In Vitro from Oxidative Stress: A Paradigm for Neuronal Cell Survival under Neurodegenerative Conditions

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Barbara Bettegazzi ◽  
Ilaria Pelizzoni ◽  
Floramarida Salerno Scarzella ◽  
Lisa Michelle Restelli ◽  
Daniele Zacchetti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Mitochondrial Dynamics ◽  
Neuronal Cell ◽  
The Other ◽  
Antioxidant Defenses ◽  
Glutathione Depletion ◽  
Other Hand ◽  
Peroxiredoxin 3

Several neurodegenerative disorders exhibit selective vulnerability, with subsets of neurons more affected than others, possibly because of the high expression of an altered gene or the presence of particular features that make them more susceptible to insults. On the other hand, resilient neurons may display the ability to develop antioxidant defenses, particularly in diseases of mitochondrial origin, where oxidative stress might contribute to the neurodegenerative process. In this work, we investigated the oxidative stress response of embryonic fibroblasts and cortical neurons obtained from Afg3l2-KO mice. AFG3L2 encodes a subunit of a protease complex that is expressed in mitochondria and acts as both quality control and regulatory enzyme affecting respiration and mitochondrial dynamics. When cells were subjected to an acute oxidative stress protocol, the survival of AFG3L2-KO MEFs was not significantly influenced and was comparable to that of WT; however, the basal level of the antioxidant molecule glutathione was higher. Indeed, glutathione depletion strongly affected the viability of KO, but not of WT MEF, thereby indicating that oxidative stress is more elevated in KO MEF even though well controlled by glutathione. On the other hand, when cortical KO neurons were put in culture, they immediately appeared more vulnerable than WT to the acute oxidative stress condition, but after few days in vitro, the situation was reversed with KO neurons being more resistant than WT to acute stress. This compensatory, protective competence was not due to the upregulation of glutathione, rather of two mitochondrial antioxidant proteins: superoxide dismutase 2 and, at an even higher level, peroxiredoxin 3. This body of evidence sheds light on the capability of neurons to activate neuroprotective pathways and points the attention to peroxiredoxin 3, an antioxidant enzyme that might be critical for neuronal survival also in other disorders affecting mitochondria.

The Nephroprotective Role of Carnosine Against Ifosfamide-Induced Renal Injury and Electrolytes Imbalance is Mediated Via the Regulation of Mitochondrial Function and Alleviation of Oxidative Stress

Drug Research ◽  
2019 ◽  
Vol 70 (01) ◽  
pp. 49-56 ◽  
Author(s):  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Vahid Ghanbarinejad ◽  
Hamid Reza Mohammadi ◽  
Mousavi Khadijeh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Renal Injury ◽  
Elevated Serum ◽  
Renal Tissue ◽  
Experimental Models ◽  
Kidney Mitochondria ◽  
Urine Biomarkers ◽  
Markers Of Oxidative Stress

Abstract Background Ifosfamide (IFO) is an alkylating agent administered against different types of malignancies. Several cases of renal injury and serum electrolytes disturbances have been reported in IFO-treated patients. Oxidative stress and mitochondrial dysfunction are suspected of being involved in the mechanism of IFO nephrotoxicity. Carnosine is a dipeptide which its antioxidant and mitochondria protecting properties have been mentioned in different experimental models. The current study aimed to evaluate the nephroprotective properties of carnosine against IFO-induced renal injury. Methods Rats were treated with IFO (50 mg/kg, i.p) alone or in combination with carnosine. Serum and urine biomarkers of renal injury in addition to kidney markers of oxidative stress were evaluated. Moreover, kidney mitochondria were isolated, and some mitochondrial indices were assessed. Results Elevated serum creatinine and BUN, hypokalemia, and hypophosphatemia, in addition, to an increase in urine glucose, protein, γ-GT, and alkaline phosphatase (ALP), were evident in IFO-treated animals. IFO also caused an increase in kidney reactive oxygen species (ROS) and lipid peroxidation (LPO). Renal GSH levels and antioxidant capacity were also depleted with IFO therapy. Mitochondrial dehydrogenase activity, GSH level, membrane potential, and ATP content were decreased while mitochondrial LPO and permeabilization were increased in IFO group. Carnosine (250 and 500 mg/kg, i.p) mitigated IFO-induced oxidative stress and mitochondrial impairment in renal tissue. Conclusion Our data suggest mitochondrial dysfunction and oxidative stress as fundamental mechanisms of renal injury induced by IFO. On the other hand, carnosine supplementation protected kidneys against IFO-induced injury through regulating mitochondrial function and mitigating oxidative stress.

scholarly journals Boldine Supplementation Regulates Mitochondrial Function and Oxidative Stress in a Rat Model of Hepatotoxicity

2019 ◽  
Vol 25 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Reza Heidari ◽  
Mohammad Reza Arabnezhad ◽  
Mohammad Mehdi Ommati ◽  
Negar Azarpira ◽  
Elham Ghodsimanesh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Liver Tissue ◽  
Acute Liver Injury ◽  
Experimental Models ◽  
Clinical Value ◽  
Protective Properties ◽  
Markers Of Oxidative Stress ◽  
Dehydrogenases Activity ◽  
And Oxidative Stress

Background: The xenobiotics-induced liver injury is a clinical complication. Hence, finding new hepatoprotective strategies has clinical value. Oxidative stress and its subsequent complications are major mechanisms involved in xenobiotics-induced hepatotoxicity. Boldine is one of the most potent antioxidant molecules widely investigated for its protective properties in different experimental models. In the current study, the hepatoprotective properties of boldine and its potential mechanisms of hepatoprotection have been investigated. Methods: Rats received thioacetamide (TAA; 200 mg/kg, i.p) as a model of acute liver injury. Boldine (5, 10, 1nd 20 mg/kg; 24 hours intervals; oral) was administered as the hepatoprotective agent. Results: Liver injury was evident in TAA-treated animals (48 hours after TAA exposure) as a severe increase in serum level of liver injury biomarkers and histopathological alterations. Moreover, markers of oxidative stress were increased in liver tissue of TAA-treated rats. Assessment of mitochondrial indices of functionality revealed a significant decrease in mitochondrial dehydrogenases activity, the collapse of mitochondrial membrane potential, mitochondrial swelling and depletion of ATP content. It was found that boldine supplementation mitigated liver tissue markers of oxidative stress and improved mitochondrial indices of functionality in TAA-treated animals. Conclusion: The hepatoprotective properties of boldine might primarily rely on antioxidant and mitochondria protecting effects of this alkaloid.

Reflecting Muslim-Christian Relations In Community Of Tegalrejo, Babadan-Ngancar-Kediri, 2019: Confronting Post-Truth

2021 ◽  
Vol 24 (1) ◽  
pp. 155-170
Author(s):  
Abdullah Muslich Rizal Maulana ◽  
Asep Awaludin ◽  
Afif Gita Fauzi ◽  
Afif Gita Fauzi
Keyword(s):  
Data Analysis ◽  
Family Environment ◽  
Essential Element ◽  
Field Research ◽  
External Factors ◽  
The Other ◽  
Mutual Respect ◽  
Internal Factors ◽  
Christian Communities ◽  
Other Hand

An interreligious harmony is particularly desired nowadays concerning recent ‘Post Truth’ era where a ‘truth' is challenged to ‘coexist’ altogether as an essential element of mankind. In Indonesia, there are beautiful neighborhoods displaying interreligious peace as a fact should be reflected further to display tolerance embedded within its society. One of these instances is Hamlet of Tegalrejo. This communitry is located in Village of Babadan, Sub-District of Ngancar, Kediri Regency. In this region, both Muslim and Christian communities live in harmony without any notable historical conflict. This research intended to conceal factors of interreligious harmony behind Tegalrejo society in a form of ‘Field Research’ through data analysis of interviews, observation, and documentations. This paper, furthermore, will be ended with an addition of reflection regarding the concept of al-‘Ta’āyush as basis of interreligious harmony in Worldview of Islam. The result of this study is that there are both external and internal factors accomplishing interreligious harmony in Tegalrejo. External factors consist community and family environment altogether with an interrelationship between its occupants. Internal factors, in the other hand, encompass mutual respect and understanding between Tegalrejo community.

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