Paraquat induces oxidative stress, neuronal loss in substantia nigra region and Parkinsonism in adult rats: Neuroprotection and amelioration of symptoms by water-soluble formulation of Coenzyme Q10

Background: Busulfan (Bu) is an anticancer drug with a variety of adverse effects for cancer patients. Oxidative stress has been considered as a common pathological mechanism and it has a key role in the initiation and progression of liver injury by Bu. Aim: The study aimed to evaluate the antioxidant impact of L-Carnitine and Coenzyme Q10 and their protective role against oxidative stress damage in liver tissues. Methods and Material: Thirty-six albino rats were divided equally into six groups. G1 (con), received I.P. injection of DMSO plus 1 ml of distilled water daily by oral gavages; G2 (Bu), received I.P. injection of Bu plus 1 ml of the distilled water daily; G3 (L-Car), received 1 ml of L-Car orally; G4 (Bu + L-Car) received I.P. injection of Bu plus 1 ml of L-Car, G5 (CoQ10) 1 ml of CoQ10 daily; and G6 (Bu + CoQ10) received I.P. injection of Bu plus 1 ml of CoQ10 daily. Results: The recent data showed that Bu induced significant (P<0.05) elevation in serum ALT, AST, liver GSSG, NO, MDA and 8-OHDG, while showing significant (P<0.05) decrease in liver GSH and ATP. On the other hand, L-Carnitine and Coenzyme Q10 ameliorated the negative effects prompted by Bu. Immunohistochemical expression of caspase-3 in liver tissues reported pathological alterations in Bu group while also showed significant recovery in L-Car more than CoQ10. Conclusion: L-Car, as well as CoQ10, can enhance the hepatotoxic effects of Bu by promoting energy production in oxidative phosphorylation process and by scavenging the free radicals.

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Beneficial Effects of Coenzyme Q10 in Reduction of Testicular Tissue Alteration Following Induction of Diabetes in Adult Rats

Romanian Journal of Diabetes Nutrition and Metabolic Diseases ◽

10.1515/rjdnmd-2015-0003 ◽

2015 ◽

Vol 22 (1) ◽

pp. 19-27 ◽

Cited By ~ 1

Author(s):

Davoud Kianifard ◽

Farhad Rezaee

Keyword(s):

Oxidative Stress ◽

Coenzyme Q10 ◽

Testicular Tissue ◽

Diabetic Rats ◽

Antioxidant Compounds ◽

Adult Rats ◽

Blood Concentrations ◽

Sperm Analysis ◽

Beneficial Effects ◽

Positive Effects

AbstractBackground and Aims: Various types of infertility are associated with uncontrolled hyperglycemia and diabetes. Development of oxidative stress is one the most important factors in the alteration of spermatogenesis in diabetic conditions. Consequently, the reduction of oxidative stress with antioxidant compounds can be effective in the reduction of tissue alterations. The aim of this study was to evaluate the efficacy of coenzyme Q10 in improvement of spermatogenesis in adult diabetic rats. Material and Methods: 32 adult rats were divided into four groups of control and treatment. Coenzyme Q10 (10 mg/kg body weight - b.w.) was administrated to one control and one diabetic (intraperitoneal injection of 45 mg/kg b.w. of Streptozotocin) groups. Blood concentrations of FSH, LH and Testosterone were measured. Histology of testicular tissue and sperm analysis were considered for evaluation of spermatogenesis. Results: Administration of Coenzyme Q10 led to increase of pituitary gonadotropins levels in diabetic rats. Testosterone levels were not changed significantly. Testicular morphology, spermatogenic indices and sperm analysis were improved in treated diabetic rats. Conclusions: The results of this study suggest that the use of Coenzyme Q10 has positive effects in reduction of spermatogenic alterations following induction of experimental diabetes in rats.

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Paraquat induces oxidative stress and neuronal cell death; neuroprotection by water-soluble Coenzyme Q10

Toxicology and Applied Pharmacology ◽

10.1016/j.taap.2004.04.019 ◽

2004 ◽

Vol 201 (1) ◽

pp. 21-31 ◽

Cited By ~ 137

Author(s):

S. McCarthy ◽

M. Somayajulu ◽

M. Sikorska ◽

H. Borowy-Borowski ◽

S. Pandey

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Coenzyme Q10 ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Water Soluble

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Oxidative Stress in The Hippocampus During Experimental Seizures Can Be Ameliorated With The Antioxidant Ascorbic Acid

Oxidative Medicine and Cellular Longevity ◽

10.4161/oxim.2.4.8876 ◽

2009 ◽

Vol 2 (4) ◽

pp. 214-221 ◽

Cited By ~ 52

Author(s):

Ítala Mônica Sales Santos ◽

Adriana da Rocha Tomé ◽

Gláucio Barros Saldanha ◽

Paulo Michel Pinheiro Ferreira ◽

Gardenia Carmem Gadelha Militão ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Ascorbic Acid ◽

Superoxide Dismutase ◽

Water Soluble ◽

Control Group ◽

Antioxidant Compounds ◽

Protective Effects ◽

Neuroprotective Effects ◽

Adult Rats

Ascorbic acid has many nonenzymatic actions and is a powerful water-soluble antioxidant. It protects low density lipoproteins from oxidation and reduces harmful oxidants in the central nervous system. Pilocarpine-induced seizures have been suggested to be mediated by increases in oxidative stress. Current studies have suggested that antioxidant compounds may afford some level of neuroprotection against the neurotoxicity of seizures. The objective of the present study was to evaluate the neuroprotective effects of ascorbic acid (AA) in rats, against the observed oxidative stress during seizures induced by pilocarpine. Wistar rats were treated with 0.9% saline (i.p., control group), ascorbic acid (500 mg/kg, i.p., AA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of ascorbic acid (500 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before of administration of ascorbic acid (AA plus pilocarpine group). After the treatments all groups were observed for 6 h. The enzyme activities as well as the lipid peroxidation and nitrite concentrations were measured using spectrophotometric methods and the results compared to values obtained from saline and pilocarpine-treated animals. Protective effects of ascorbic acid were also evaluated on the same parameters. In pilocarpine group there was a significant increase in lipid peroxidation and nitrite level. However, no alteration was observed in superoxide dismutase and catalase activities. Antioxidant treatment significantly reduced the lipid peroxidation level and nitrite content as well as increased the superoxide dismutase and catalase activities in hippocampus of adult rats after seizures induced by pilocarpine. Our findings strongly support the hypothesis that oxidative stress in hippocampus occurs during seizures induced by pilocarpine, proving that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and also imply that a strong protective effect could be achieved using ascorbic acid.

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Oxidative stress status in liver mitochondria and lymphocyte DNA damage of atherosclerotic rabbits supplemented with water soluble coenzyme Q10

BioFactors ◽

10.1002/biof.5520320131 ◽

2008 ◽

Vol 32 (1-4) ◽

pp. 263-273 ◽

Cited By ~ 15

Author(s):

M. Carmen Ramirez-Tortosa ◽

Sergio Granados ◽

Cesar L. Ramirez-Tortosa ◽

Julio J. Ochoa ◽

Pedro Camacho ◽

...

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Coenzyme Q10 ◽

Liver Mitochondria ◽

Water Soluble ◽

Oxidative Stress Status

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Coenzyme Q10 Attenuates Cisplatin-induced Nephrotoxicity Through Counteracting Oxidative Stress and Inflammation

Clinical Cancer Drugs ◽

10.2174/2212697x06666190701113043 ◽

2019 ◽

Vol 6 (1) ◽

pp. 41-47

Author(s):

Hala S. Bash ◽

Ihsan S. Rabeea

Keyword(s):

Oxidative Stress ◽

Serum Creatinine ◽

Coenzyme Q10 ◽

Kidney Injury ◽

Treated Group ◽

Control Group ◽

Histopathological Analysis ◽

Adult Rats ◽

Necrosis Factor Alpha ◽

Kidney Injury Molecule 1

Background: Cisplatin is an anticancer drug used in the management of solid tumors, however, dose-related nephrotoxicity is one of its major problems. Agents having antioxidants, antiinflammatory and/or antiapoptotic activities may thus represent potential therapeutic options to avoid cisplatin-induced nephrotoxicity. Among these agents, coenzyme Q10 has several pharmacological properties including antioxidant, anti-inflammatory and/or anti-apoptotic effects. Objective: The current study aimed to examine whether coenzyme Q10 could attenuate cisplatininduced nephrotoxicity or not. Methods: 24 adult rats were randomly separated into three groups (8 rats per group). The first one was the control group, rats receiving vehicle (olive oil) intraperitoneally. The second group was Cisplatin treated group, rats were receiving 13 mg/kg of Cisplatin intraperitoneally as a single dose. The third group (Cisplatin + Coenzyme Q10), rats were receiving 13 mg/kg as a single intraperitoneal dose of Cisplatin and coenzyme Q10 daily for six consecutive days (10 mg/kg intraperitoneally). Results: Cisplatin caused significant increases in serum creatinine and severe histological lesions. Cisplatin treated group also showed a significant elevation in renal malondialdehyde concentration as a marker of oxidative stress; renal tumor necrosis factor-alpha concentration as a marker of inflammation; and Kidney injury molecule -1 concentration. Coenzyme Q10 significantly attenuated cisplatininduced nephrotoxicity through lowering serum creatinine and improving nephrotoxicity histological scores. Coenzyme Q10 also significantly reduced the renal concentration of MDA, TNF-α and KIM-1 relative to cisplatin treated group. Conclusions: Coenzyme Q10 has a potential nephroprotective effect against cisplatin-induced nephrotoxicity that was demonstrated by biochemical and histopathological analysis.

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Physical exercise protects dynamic balance and motor coordination of rats treated with vincristine

Revista Brasileira de Fisiologia do Exercício ◽

10.33233/rbfex.v19i5.4220 ◽

2020 ◽

Vol 19 (5) ◽

pp. 336

Author(s):

Luiza Minato Sagrillo ◽

Viviane Nogueira De Zorzi ◽

Luiz Fernando Freire Royes ◽

Michele Rechia Fighera ◽

Beatriz Da Silva Rosa Bonadiman ◽

...

Keyword(s):

Oxidative Stress ◽

Locomotor Activity ◽

Physical Exercise ◽

Motor Coordination ◽

Dynamic Balance ◽

Exercise Group ◽

Adult Rats ◽

The Central Nervous System ◽

Stress Damage ◽

Training Protocol

Physical exercise has been shown to be an important modulator of the antioxidant system and neuroprotective in several diseases and treatments that affect the central nervous system. In this sense, the present study aimed to evaluate the effect of physical exercise in dynamic balance, motor coordination, exploratory locomotor activity and in the oxidative and immunological balance of rats treated with vincristine (VCR). For that, 40 adult rats were divided into two groups: exercise group (6 weeks of swimming, 1h/day, 5 days/week, with overload of 5% of body weight) and sedentary group. After training, rats were treated with 0.5 mg/kg of vincristine sulfate for two weeks or with the same dose of 0.9% NaCl. The behavioral tests were conducted 1 and 7 days after each dose of VCR. On day 15 we carried out the biochemical analyzes of the cerebellum. The physical exercise was able to protect against the loss of dynamic balance and motor coordination and, had effect per se in the exploratory locomotor activity, and neutralize oxidative stress, damage DNA and immune damage caused by VCR up to 15 days after the end of the training protocol. In conclusion, we observed that previous physical training protects of the damage motor induced by vincristine.Key-words: exercise, oxidative stress, neuroprotection, cerebellum.

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Novel Insights into the Regulatory Role of Nuclear Factor (Erythroid-Derived 2)-Like 2 in Oxidative Stress and Inflammation of Human Fetal Membranes

International Journal of Molecular Sciences ◽

10.3390/ijms21176139 ◽

2020 ◽

Vol 21 (17) ◽

pp. 6139 ◽

Cited By ~ 1

Author(s):

Ramkumar Menon ◽

Morgan R Peltier

Keyword(s):

Oxidative Stress ◽

Heme Oxygenase ◽

Water Soluble ◽

Fetal Membrane ◽

Fetal Membranes ◽

Peroxisome Proliferator ◽

Nuclear Factor ◽

Western Blots ◽

Adverse Pregnancy ◽

Nrf2 Expression

Fetal membrane dysfunction in response to oxidative stress (OS) is associated with adverse pregnancy outcomes. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is one of the regulators of innate OS response. This study evaluated changes in Nrf2 expression and its downstream targets heme oxygenase (HO-1) and peroxisome proliferator-activated receptor gamma (PPARγ) in fetal membranes during OS and infection in vitro. Furthermore, we tested the roles of sulforaphane (SFN; an extract from cruciferous vegetables) and trigonelline (TRN; an aromatic compound in coffee) in regulating Nrf2 and its targets. Fetal membranes (n = 6) collected at term were placed in an organ explant system were treated with water-soluble cigarette smoke extract (CSE), an OS inducer (1:10), and lipopolysaccharide (LPS; 100 ng/mL). Nrf2 expression, expression, its enhancement by sulforaphane (SFN, 10 µM/mL) and down regulation by TRN (10uM/mL) was determined by western blots. Expression of Nrf2 response elements PPARγ (western) heme oxygenase (HO-1), and IL-6 were quantified by ELISA. CSE and LPS treatment of fetal membranes increased nrf2, but reduced HO-1 and PPARγ and increased IL-6. Co-treatment of SFN, but not with TRN, with CSE and LPS increased Nrf2 substantially, as well as increased HO-1 and PPARγ and reduced IL-6 expression. Risk factor-induced Nrf2 increase is insufficient to generate an antioxidant response in fetal membranes. Sulforaphane may enhance innate antioxidant and anti-inflammatory capacity by increasing NRF-2 expression.

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Comparison of coenzyme Q10 or fish oil for prevention of intermittent hypoxia-induced oxidative injury in neonatal rat lungs

Respiratory Research ◽

10.1186/s12931-021-01786-w ◽

2021 ◽

Vol 22 (1) ◽

Author(s):

Christina D’Agrosa ◽

Charles L. Cai ◽

Faisal Siddiqui ◽

Karen Deslouches ◽

Stephen Wadowski ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Lung Injury ◽

Fish Oil ◽

Coenzyme Q10 ◽

Intermittent Hypoxia ◽

Oxidative Injury ◽

Adverse Outcomes ◽

Neonatal Rat ◽

Antioxidant Systems

Abstract Background Neonatal intermittent hypoxia (IH) results in oxidative distress in preterm infants with immature antioxidant systems, contributing to lung injury. Coenzyme Q10 (CoQ10) and fish oil protect against oxidative injury. We tested the hypothesis that CoQ10 is more effective than fish oil for prevention of IH-induced lung injury in neonatal rats. Methods Newborn rats were exposed to two clinically relevant IH paradigms at birth (P0): (1) 50% O2 with brief hypoxia (12% O2); or (2) room air (RA) with brief hypoxia (12% O2), until P14 during which they were supplemented with daily oral CoQ10, fish oil, or olive oil from P0 to P14. Pups were studied at P14 or placed in RA until P21 with no further treatment. Lungs were assessed for histopathology and morphometry; biomarkers of oxidative stress and lipid peroxidation; and antioxidants. Results Of the two neonatal IH paradigms 21%/12% O2 IH resulted in the most severe outcomes, evidenced by histopathology and morphometry. CoQ10 was effective for preserving lung architecture and reduction of IH-induced oxidative stress biomarkers. In contrast, fish oil resulted in significant adverse outcomes including oversimplified alveoli, hemorrhage, reduced secondary crest formation and thickened septae. This was associated with elevated oxidants and antioxidants activities. Conclusions Data suggest that higher FiO2 may be needed between IH episodes to curtail the damaging effects of IH, and to provide the lungs with necessary respite. The negative outcomes with fish oil supplementation suggest oxidative stress-induced lipid peroxidation.

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Intermittent Hypobaric Hypoxic Preconditioning Provides Neuroprotection by Increasing Antioxidant Activity, Erythropoietin Expression and Preventing Apoptosis and Astrogliosis in the Brain of Adult Rats Exposed to Acute Severe Hypoxia

International Journal of Molecular Sciences ◽

10.3390/ijms22105272 ◽

2021 ◽

Vol 22 (10) ◽

pp. 5272

Author(s):

Débora Coimbra-Costa ◽

Fernando Garzón ◽

Norma Alva ◽

Tiago C. C. Pinto ◽

Fernando Aguado ◽

...

Keyword(s):

Oxidative Stress ◽

Hypobaric Hypoxia ◽

Hypoxic Preconditioning ◽

Severe Hypoxia ◽

Efficient Tool ◽

Adult Rats ◽

Therapeutic Benefits ◽

Background Exposure ◽

The Brain ◽

Apoptotic Cascade

Background: Exposure to intermittent hypoxia has been demonstrated to be an efficient tool for hypoxic preconditioning, preventing damage to cells and demonstrating therapeutic benefits. We aimed to evaluate the effects of respiratory intermittent hypobaric hypoxia (IHH) to avoid brain injury caused by exposure to acute severe hypoxia (ASH). Methods: biomarkers of oxidative damage, mitochondrial apoptosis, and transcriptional factors in response to hypoxia were assessed by Western blot and immunohistochemistry in brain tissue. Four groups of rats were used: (1) normoxic (NOR), (2) exposed to ASH (FiO2 7% for 6 h), (3) exposed to IHH for 3 h per day over 8 days at 460 mmHg, and (4) ASH preconditioned after IHH. Results: ASH animals underwent increased oxidative-stress-related parameters, an upregulation in apoptotic proteins and had astrocytes with phenotype forms compatible with severe diffuse reactive astrogliosis. These effects were attenuated and even prevented when the animals were preconditioned with IHH. These changes paralleled the inhibition of NF-κB expression and the increase of erythropoietin (EPO) levels in the brain. Conclusions: IHH exerted neuroprotection against ASH-induced oxidative injury by preventing oxidative stress and inhibiting the apoptotic cascade, which was associated with NF-κB downregulation and EPO upregulation.

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