Dual effects of sulfasalazine on rat sperm characteristics, spermatogenesis, and steroidogenesis in two experimental models

Ommati, Mohammad Mehdi; Heidari, Reza; Jamshidzadeh, Akram; Zamiri, Mohammad Javad; Sun, Zilong; Sabouri, Samira; Wang, Jundong; Ahmadi, Fatemeh; Javanmard, Nafiseh; Seifi, Kazem; Mousapour, Saeed; Yeganeh, Babak Shirazi

doi:10.1016/j.toxlet.2017.11.034

Cited by 61 publications

(26 citation statements)

References 53 publications

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“…Briefly, a mitochondrial suspension (1 mg protein/mL) was incubated with MTT (40 μL of 0.4% w: v solution) for 30 min (37 °C in the dark). The product of purple formazan crystals was dissolved in dimethyl sulfoxide (DMSO, 1 mL) and the optical density (OD) was measured (λ = 570 nm, EPOCH plate reader, Bio-Tek ® Instruments, Highland Park, USA) (Heidari and Niknahad, 2019; Ommati et al., 2018).…”

Section: Methodsmentioning

confidence: 99%

“…A luciferase-luciferin-based kit (Enliten ® from Promega, Madison, USA) was used to assess mitochondrial ATP content (Heidari et al., 2018b; Ommati et al., 2018). Samples and buffer solutions were prepared based on the kit instructions.…”

Section: Methodsmentioning

confidence: 99%

“…Briefly, mitochondrial samples (500 μL, 1 mg protein/mL) were treated with 200 μL of ice-cooled TCA solution (0.3% w: v in MiliQ water, 4 °C) and centrifuged (15,000 g , 15 min, 4 °C). Afterward, 100 μL of the supernatant was treated with 100 μL of ATP kit content in the dark, and the luminescence intensity of samples was measured (λ = 560 nm, FLUOstar Omega ® multifunctional microplate reader, BMG Labtech Inc., Ortenberg, Germany) (Heidari et al., 2018b; Ommati et al., 2018).…”

Section: Methodsmentioning

confidence: 99%

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The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury

Emadi

Abdoli

Ghanbarinejad

et al. 2019

Heliyon

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Imatinib is a tyrosine kinase inhibitor widely administered against chronic myeloid leukemia. On the other hand, drug-induced kidney proximal tubular injury, electrolytes disturbances, and renal failure is a clinical complication associated with imatinib therapy. There is no precise cellular mechanism(s) for imatinib-induced renal injury. The current investigation aimed to evaluate the role of mitochondrial dysfunction and oxidative stress in the pathogenesis of imatinib nephrotoxicity. Rats received imatinib (50 and 100 mg/kg, oral, 14 consecutive days). Serum and urine biomarkers of renal injury and markers of oxidative stress in the kidney tissue were assessed. Moreover, kidney mitochondria were isolated, and mitochondrial indices, including mitochondrial depolarization, dehydrogenases activity, mitochondrial permeabilization, lipid peroxidation (LPO), mitochondrial glutathione levels, and ATP content were determined. A significant increase in serum (Creatinine; Cr and blood urea nitrogen; BUN) and urine (Glucose, protein, gamma-glutamyl transferase; γ-GT, and alkaline phosphatase; ALP) biomarkers of renal injury, as well as serum electrolytes disturbances (hypokalemia and hypophosphatemia), were evident in imatinib-treated animals. On the other hand, imatinib (100 mg/kg) caused an increase in kidney ROS and LPO. Renal tubular interstitial nephritis, tissue necrosis, and atrophy were evident as tissue histopathological changes in imatinib-treated rats. Mitochondrial parameters were also adversely affected by imatinib administration. These data represent mitochondrial impairment, renal tissue energy crisis, and oxidative stress as possible mechanisms involved in the pathogenesis of imatinib-induced renal injury and serum electrolytes disturbances.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury

Emadi

Abdoli

Ghanbarinejad

et al. 2019

Heliyon

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“…37,38 Then, samples were centrifuged (15 000 g, 5 minutes, 4°C) and the fluorescence intensity of the supernatant was measured using a multifunctional fluorescent microplate reader (FLUOstar Omega ® , BMG Labtech, Germany; λ excitation = 485 nm and λ emission = 525 nm). 33,41…”

Section: Methodsmentioning

confidence: 99%

Carnosine Mitigates Manganese Mitotoxicity in an In Vitro Model of Isolated Brain Mitochondria

et al. 2019

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Purpose: Manganese (Mn) is a neurotoxic chemical which induces a wide range of complications in the brain tissue. Impaired locomotor activity and cognitive dysfunction are associated with high brain Mn content. At the cellular level, mitochondria are potential targets for Mn toxicity. Carnosine is a dipeptide abundantly found in human brain. Several pharmacological properties including mitochondrial protecting and antioxidative effects have been attributed to carnosine. The current study aimed to evaluate the effect of carnosine treatment on Mn-induced mitochondrial dysfunction in isolated brain mitochondria. Methods: Mice brain mitochondria were isolated based on the differential centrifugation method and exposed to increasing concentrations of Mn (10 µM-10 mM). Carnosine (1 mM) was added as the protective agent. Mitochondrial indices including mitochondrial depolarization, reactive oxygen species (ROS) formation, mitochondrial dehydrogenases activity, ATP content, and mitochondrial swelling and permeabilization were assessed. Results: Significant deterioration in mitochondrial indices were evident in Mn-exposed brain mitochondria. On the other hand, it was found that carnosine (1 mM) treatment efficiently prevented Mn-induced mitochondrial impairment. Conclusion: These data propose mitochondrial protection as a fundamental mechanism for the effects of carnosine against Mn toxicity. Hence, this peptide might be applicable against Mn neurotoxicity with different etiologies (e.g., in cirrhotic patients).

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“…Samples (0.5 mg protein/mL) were incubated with rhodamine 123 (10 µM final concentration) for 30 min (37 °C, with continuous shaking). Afterward, samples were centrifuged (15 000 g, 5 min, 4 °C) and the fluorescence intensity of the supernatant was measured (FLUOstar Omega ® multifunctional microplate reader, BMG Labtech, Germany, λ excitation = 485 nm and λ emission = 525 nm) [21].…”

Section: Mitochondrial Depolarizationmentioning

confidence: 99%

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

et al. 2019

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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.

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Dual effects of sulfasalazine on rat sperm characteristics, spermatogenesis, and steroidogenesis in two experimental models

Cited by 61 publications

References 53 publications

The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury

The potential role of mitochondrial impairment in the pathogenesis of imatinib-induced renal injury

Carnosine Mitigates Manganese Mitotoxicity in an In Vitro Model of Isolated Brain 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

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