Sulfasalazine-induced renal and hepatic injury in rats and the protective role of taurine

Heidari, Reza; Rasti, Maryam; Yeganeh, Babak Shirazi; Niknahad, Hossein; Saeedi, Arastoo; Najibi, Asma

doi:10.15171/bi.2016.01

Cited by 46 publications

(36 citation statements)

References 46 publications

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“…Besides Mtx, other DMARDs, including sulfasalazine, hydroxychloroquine, and leflunomide, shared many of the same potential toxicities as those of Mtx, including cytopenia and hepatotoxicity 39,40. However, in this study, side effects reported with the use of sulfasalazine, hydroxychloroquine, and leflunomide were less common, making up only about 20% of all the adverse reactions reported.…”

Section: Discussionmentioning

confidence: 52%

<p>Drug-related problems in patients with rheumatoid arthritis</p>

Ning¹,

Huri²,

Yahya³

2019

TCRM

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BackgroundRheumatoid arthritis (RA) patients are at risk of acquiring drug-related problems (DRPs). However, there has been a lack of studies on DRPs in patients with RA up to now.MethodThis retrospective study was conducted in a tertiary hospital in Malaysia from January 2012 to December 2017 with the purpose of assessing DRPs in RA patients and factors associated with its occurrence. A total of 200 patients who had received pharmacological treatment for RA were enrolled in this study. Assessment of DRPs was based on the Pharmaceutical Network Care Europe tool version 5.01.ResultsA total of 289 DRPs with an average of 1.5±1.0 problems per patient were identified, in which 78.5% of the population had at least one DRP. The most common DRPs encountered were adverse reactions (38.8%), drug interactions (33.6%), and drug-choice problems (14.5%). Factors that had significant association with the occurrence of DRPs were polypharmacy (P=0.003), multiple comorbidities (P=0.001), hyperlipidemia (P=0.009), osteo (P=0.040), and renal impairment (P=0.044). These data indicated that the prevalence of DRPs was high among RA patients.ConclusionEarly identification of types of DRPs and associated factors may enhance the prevention and management of RA.

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Section: Discussionmentioning

confidence: 52%

<p>Drug-related problems in patients with rheumatoid arthritis</p>

Ning¹,

Huri²,

Yahya³

2019

TCRM

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“…Blood was collected from the abdominal aorta, transferred to standard tubes (Improvacuter ® ; gel and clot activator-coated tubes; Guangzhou, China) and centrifuged (3000 g , 10 minutes, 8 °C) to prepare serum. An autoanalyzer (Mindray BS-200 ® , China) and standard kits (Pars Azmun ® , Tehran, Iran) were employed to assess serum creatinine (Cr), phosphate, uric acid, calcium, blood urea nitrogen (BUN), glucose, gamma-glutamyl transpeptidase (γ-GT), alkaline phosphatase (ALP), and protein (Heidari et al., 2016; Jamshidzadeh et al., 2015). Sodium (Na + ) and potassium (K + ) levels were measured using a flame photometer (Clinical Flame Photometer, Sherwood Scientific, UK).…”

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

Self Cite

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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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“…Similarly, taurine proved to be effective in reversing sulfasalazine-mediated effects, owing to its anti-oxidant nature. In particular, taurine was presented as a recommended option against Crohn's disease, through its inhibitory action on LPO, and GSH status in both hepatic and renal cells (158).…”

Section: Beneficial Effect Of Taurine In Various Cancers (In Vitro Anmentioning

confidence: 99%

Role of taurine, its haloamines and its lncRNA TUG1 in both inflammation and cancer progression. On the road to therapeutics? (Review)

Baliou

Kyriakopoulos²,

Spandidos

et al. 2020

Int J Oncol

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For one century, taurine is considered as an end product of sulfur metabolism. In this review, we discuss the beneficial effect of taurine, its haloamines and taurine upregulated gene 1 (TUG1) long non-coding RNA (lncRNA) in both cancer and inflammation. We outline how taurine or its haloamines (N-Bromotaurine or N-Chlorotaurine) can induce robust and efficient responses against inflammatory diseases, providing insight into their molecular mechanisms. We also provide information about the use of taurine as a therapeutic approach to cancer. Taurine can be combined with other chemotherapeutic drugs, not only mediating durable responses in various malignancies, but also circumventing the limitations met from chemotherapeutic drugs, thus improving the therapeutic outcome. Interestingly, the lncRNA TUG1 is regarded as a promising therapeutic approach, which can overcome acquired resistance of cancer cells to selected strategies. In this regard, we can translate basic knowledge about taurine and its TUG1 lncRNA into potential therapeutic options directed against specific oncogenic signaling targets, thereby bridging the gap between bench and bedside. Contents 1. The role of taurine in inflammation 2. Formation of taurine haloamines 3. Anti-microbial properties of taurine haloamines 4. Anti-inflammatory and anti-oxidant properties of taurine haloamines 5. Therapeutic perspectives and clinical studies 6. Significance of lncRNA TUG1 lncRNA in cancer 7. The association of lncRNA TUG1 and chemoresistance 8. The role of taurine or lncRNA TUG1 as a prognostic marker 9. Conclusions

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Sulfasalazine-induced renal and hepatic injury in rats and the protective role of taurine

Cited by 46 publications

References 46 publications

<p>Drug-related problems in patients with rheumatoid arthritis</p>

<p>Drug-related problems in patients with rheumatoid arthritis</p>

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

Role of taurine, its haloamines and its lncRNA TUG1 in both inflammation and cancer progression. On the road to therapeutics? (Review)

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