The Effects of Cimetidine, N-Acetylcysteine, and Taurine on Thioridazine Metabolic Activation and Induction of Oxidative Stress in Isolated Rat Hepatocytes

Eftekhari, Aziz; Ahmadian, Elham; Azarmi, Yadollah; Parvizpur, Alireza; Fard, Javad Khalili; Eghbal, Mohammad Ali

doi:10.1007/s11094-018-1724-6

Cited by 52 publications

(33 citation statements)

References 18 publications

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“…Samples were incubated in the dark (15 min, 37 °C in a shaker incubator). Finally, the fluorescence intensity (FI) of the samples was assessed using a FLUOstar Omega ® multifunctional microplate reader (BMG Labtech Inc., Germany, λ excitation = 485 nm and λ emission = 525 nm) (Socci et al., 1999; Jamshidzadeh et al., 2015; Ahmadian et al., 2018; Eftekhari et al., 2018).…”

Section: Methodsmentioning

confidence: 99%

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%

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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“…Then, the centrifugation of the sample in 15000 ×g was done for 5 min and the intensity of the dye fluorescent was recorded in the supernatant at emission and excitation wavelength of 525 and 485 nm, respectively [42].…”

Section: Mitochondrial Depolarizationmentioning

confidence: 99%

Betanin prohibits cisplatin-induced nephrotoxicity through targeting mitochondria

Vahed¹,

Ardalan²,

Khalilov³

et al. 2019

Sanat

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Cisplatin is a common chemotherapeutic agent against a wide range of solid tumors. The clinical application of cisplatin is restricted due to its adverse effect, mainly nephrotoxicity. The aim of this study was to examine whether betanin (a natural pigment) is able to alleviate cisplatin-induced renal injury. Rats received cisplatin (10 mg/kg, single dose) after 3 consecutive days of betanin (100 mg/kg) oral gavage. Serum and urine samples were collected and kidney mitochondria were isolated from the treated groups for the further evaluations. Cisplatin-treated animals revealed altered biochemical evidence of nephrotoxicity, which were significantly improved in betanin pre-treated groups. On the other hand, betanin modulated mitochondrial parameters such as mitochondrial dehydrogenase activity, mitochondrial swelling, mitochondrial ATP content, mitochondrial depolarization, lipid peroxidation, and cytochrome c release. These data propose the possible protective role of betanin in cisplatin-associated nephrotoxicity in which the mechanism appears to be a prohibition of chemical disturbances and mitochondrial damage.

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“…The antioxidant role of Tau has been mentioned as a fundamental mechanism involved in the cardioprotective effects of this amino acid [ 23 - 25 ]. It has been found that Tau protects heart tissue against toxic insults by alleviation of oxidative stress and its associated events [ 10 , 26 - 31 ]. Interestingly, recent studies mentioned that the antioxidant effect of Tau is indirectly mediated by the effects of this amino acid on cellular mitochondria [ 16 , 32 - 37 ].…”

Section: Introductionmentioning

confidence: 99%

Taurine mitigates cirrhosis-associated heart injury through mitochondrial-dependent and antioxidative mechanisms

Mousavi¹,

Niknahad²,

Mostofi³

et al. 2020

ceh

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The Effects of Cimetidine, N-Acetylcysteine, and Taurine on Thioridazine Metabolic Activation and Induction of Oxidative Stress in Isolated Rat Hepatocytes

Cited by 52 publications

References 18 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

Betanin prohibits cisplatin-induced nephrotoxicity through targeting mitochondria

Taurine mitigates cirrhosis-associated heart injury through mitochondrial-dependent and antioxidative mechanisms

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