Sulfasalazine induced oxidative stress: A possible mechanism of male infertility

Alonso, Virginia; Linares, Victòria; Bellés, Montserrat; Albina, M. Luisa; Sirvent, Juan J.; Domingo, José L.; Sánchez, Domènec J.

doi:10.1016/j.reprotox.2008.10.007

Cited by 71 publications

(45 citation statements)

References 35 publications

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“…Some investigations indicated the involvement of oxidative stress and its consequent events in this complication [8,9]. Oxidative stress and its consequences also seem to be involved in other sulfasalazine side effects including infertility and hepatic injury [40][41][42]. In line with previous investigations, we found that sulfasalazine significantly increased oxidative stress biomarkers in the kidney tissue (Table 1).…”

Section: Discussionsupporting

confidence: 90%

Sulfasalazine induces mitochondrial dysfunction and renal injury

et al. 2017

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Sulfasalazine is a commonly used drug for the treatment of rheumatoid arthritis and inflammatory bowel disease. There are several cases of renal injury encompass sulfasalazine administration in humans. The mechanism of sulfasalazine adverse effects toward kidneys is obscure. Oxidative stress and its consequences seem to play a role in the sulfasalazine-induced renal injury. The current investigation was designed to investigate the effect of sulfasalazine on kidney mitochondria. Rats received sulfasalazine (400 and 600 mg/kg/day, oral) for 14 consecutive days. Afterward, kidney mitochondria were isolated and assessed. Sulfasalazine-induced renal injury was biochemically evident by the increase in serum blood urea nitrogen (BUN), gamma-glutamyl transferase (c-GT), and creatinine (Cr). Histopathological presentations of the kidney in sulfasalazine-treated animals revealed by interstitial inflammation, tubular atrophy, and tissue necrosis. Markers of oxidative stress including an increase in reactive oxygen species (ROS) and lipid peroxidation (LPO), a defect in tissue antioxidant capacity, and glutathione (GSH) depletion were also detected in the kidney of sulfasalazine-treated groups. Decreased mitochondrial succinate dehydrogenase activity (SDA), mitochondrial depolarization, mitochondrial GSH depletion, increase in mitochondrial ROS, LPO, and mitochondrial swelling were also evident in sulfasalazine-treated groups. Current data suggested that oxidative stress and mitochondrial injury might be involved in the mechanism of sulfasalazine-induced renal injury. ARTICLE HISTORY

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Section: Discussionsupporting

confidence: 90%

Sulfasalazine induces mitochondrial dysfunction and renal injury

et al. 2017

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“…So sulfasalazine has the effect on raising free-radicals and RBC membrane-lipid defect. [16] One of these, is production of lipid peroxidant that decreases membrane mobility and transmembrane remission defect [10 ] Therefore, sulfasalazine has the negative effect on RBC membrane stability. In one research the effect of pissum sativum L on colitis which created by DSS (Dextrane Sodium Solphate) has been studied, and showed that pissum sativum L and its albumin part extract is BBI (Bowman-Birk Inhibitor) that care the harms of DSS.…”

Section: Discussionmentioning

confidence: 99%

Study of the Protective Effect of English pea (Pissum Sativum L) Seed Hydroethanolic Extract on Red Blood Cell Membrane Stability in Blood Samples Exposed to Sulfasalazine

2016

2016 International Conference on Biological and Environmental Science (BIOES-16) June 8-9, 2016 New Jersey (USA)

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Abstract:In this laboratory experimental study we assessed antioxidant effect of pea (Pissum sativum L)extract on RBC membrane stability. For this purpose, human blood samples were used in our study and exposed to different doses of extract in blood cells that were previously exposed to sulfasalazine. ANOVA used to analyze the data. Our results showed that administration pissum sativum L extract (2,4,6,mg/kg) led to increase in RBC membrane stability and neutralized the effect of sulfasalazine.

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“…In particular, sulphasalazine and sulphonamide drugs, substrates for NAT2, are able to depress sperm motility and acrosome reaction by means of increasing oxidative stress (Alonso et al, 2009;Fukushima et al, 2005).…”

Section: Discussionmentioning

confidence: 99%