Assessment of the pro-oxidant activity of uranium in kidney and testis of rats

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

doi:10.1016/j.toxlet.2006.09.004

Cited by 76 publications

(52 citation statements)

References 46 publications

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“…Chez le rongeur, suite à une exposition aiguë, à raison de 0,5 à 5 mg/kg en injection intrapéritonéale unique, une variation au niveau rénal de l'expression des enzymes antioxydantes (SOD, catalase…) et une augmentation de la peroxydation lipidique sont observées (Banday et al, 2008a ;Belles et al, 2007 ;Priyamvada et al, 2010). Chez le rat, après exposition chronique (3 mois, 40 mg/kg) l'uranium induit une augmentation de marqueurs du stress oxydant (peroxydation lipidique et oxydation du glutathion (GSSG)) au niveau rénal (Linares et al, 2006). In vitro, sur des cellules rénales en culture, une augmentation de la production d'espèces réactives de l'oxygène est également observée et impliquerait une entrée des cellules en apoptose à partir de concentrations élevées (>600 µM) (Thiebault et al, 2007).…”

Section: Stress Oxydantunclassified

Données nouvelles sur la néphrotoxicité de l’uranium

Guéguen

Rouas

2012

Radioprotection

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RÉSUMÉL'uranium est un radioélément ainsi qu'un métal lourd auquel l'homme peut être exposé du fait de sa présence dans l'environnement ou des activités humaines. Il exerce principalement une toxicité chimique au niveau du tubule contourné proximal du rein après exposition aiguë ou chronique. Après exposition à une forte dose d'uranium, la néphrite tubulaire aiguë est révélée par une protéinurie ainsi qu'une diminution du débit de filtration glomérulaire. Plus récemment, l'utilisation de marqueurs d'intégrité tissulaire telle que la béta 2-microglobuline ou des enzymes tissulaires a pu être corrélée aux altérations histopathologiques des tubules contournés proximaux. Lors d'exposition chronique à de faible niveau, l'utilisation de marqueurs plus spécifiques et plus sensibles s'avère nécessaire lorsque les lésions sont faibles. Des études expérimentales développées au laboratoire ont montré la pertinence de certains de ces biomarqueurs tel que Kim-1 pour détecter de faibles altérations rénales. L'uranium exerce sa cytotoxicité au niveau des cellules épithéliales des tubules contournés proximaux probablement du fait de son entrée dans la cellule où il s'accumule préférentiellement dans le noyau cellulaire, lorsqu'il n'est pas sous forme de précipités. Les mécanismes conduisant à la mort des cellules ne sont pas encore totalement élucidés mais le stress oxydant semble y jouer un rôle important. ABSTRACT New data on uranium nephrotoxicity.Uranium is an element and also a heavy metal to which humans can be exposed due to its natural presence or human activities. It has mainly a chemical toxicity on the proximal convoluted tubules of the kidney after acute or chronic exposure. At high dose exposure, acute tubular nephritis is observed, as indicated by proteinuria and a decreased glomerular filtration rate. More recently, the use of structural biomarkers such as beta 2-microglobuline or tubular enzymes has been correlated with histopathological injury of the proximal convoluted tubules. During chronic exposure at a low level, the use of some of these sensitive and specific biomarkers would be necessary, particularly when the injury is slight. Recent experimental studies in the laboratory have shown the relevance of such new biomarkers as Kim-1 to detect slight renal injury. Uranium exerts its toxicity on epithelial tubular cells in which it accumulates mainly in the nucleus when it is not precipitated. The mechanisms leading to cell death are not totally elucidated but oxidative stress seems to play an important role.

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Section: Stress Oxydantunclassified

Données nouvelles sur la néphrotoxicité de l’uranium

Guéguen

Rouas

2012

Radioprotection

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“…Our results were in agreement with that reported by Cohen et al (1998) who concluded that PCM induced oxidative stress results in lipid peroxidation, protein thiols oxidation, depletion of antioxidant enzyme and mitochondrial endoplasmic reticulum injury. In the same line, Linares et al (2006) suggested that, during renal injury and inflammation, superoxide and peroxide radicals are generated at the site of damage, resulting in the depletion of SOD and CAT activities which are considered the most important enzymes involved in ameliorating the effects of oxygen metabolism.…”

Section: Discussionmentioning

confidence: 99%

Impact of Dehydroepiandrosterone in Prevention of Paracetamol Induced Nephrotoxicity in Rats

El-Karib¹

2014

American Medical Journal

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Paracetamol (PCM) overdose can cause nephrotoxicity with oxidative stress as one of the possible mechanisms mediating the event. However, Dehydroepiandrosterone (DHEA), the major secretory product of the human adrenal gland, has been shown to possess a multi-targeted antioxidant activity which is also effective against lipid peroxidation induced in various animal models and against various human disorders. In this study, the preventive effect of DHEA against PCM-induced nephrotoxicity was examined. Rats were divided into four groups containing 10 rats each, as follows: A control: Received normal saline, Vehicle treated: Received the vehicle (5% DMSO), PCM model (750 mg kg ), respectively, for 4 consecutive weeks. All treatment were given orally to animals. Our results show that co-treatment of DHEA with PCM prevented the PCM-induced nephrotoxicity and oxidative impairments of the kidney, as evidenced by a significantly reduced (p<0.05) level of serum creatinine, urea and BUN with parallel significant increases in serum protein, Cr clearance and kidneys weights. Furthermore, DHEA was able to induce a significant increment (p<0.05) of renal levels of reduced Glutathione (GSH) and activities of Superoxide Dismutase (SOD) and Glutathione Peroxidise (GPx). An effect that was accompanied with a significant decrease in renal lipid peroxides levels (MDA). The nephroprotective effects of DHEA was confirmed by a reduced intensity of renal cellular damage, as evidenced by histological findings. In conclusion, DHEA at a daily dose of 250 mg kg −1 has a protective role against PCM-induced nephrotoxicity in rats and the process is probably mediated through its antioxidant properties.

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“…The third hypothesis is an inhibitory effect of uranium induced oxidative stress. In fact, oxidative stress has been observed following uranium contamination in different systems (Linares et al, 2006;Periyakaruppan et al, 2007;Tasat et al, 2007). Here again, similarity between uranium and lead may be noticed because lead-induced oxidative stress has been shown as causing NO inactivation (Vaziri & Ding, 2001).…”

Section: The Nitric Oxide (No) Pathwaymentioning

confidence: 94%