Details

Autor(en) / Beteiligte

• Conterato, Greicy M. M.
• Quatrin, Andréia
• Somacal, Sabrina
• Ruviaro, Amanda R.
• Vicentini, Juliana
• Augusti, Paula R.
• Sobieski, Rocheli
• Figueiredo, Cassieli
• dos Santos, Clarissa M. M.
• Pereira, Talita C. B.
• Bogo, Maurício R.
• Flores, Erico M. M.
• Emanuelli, Tatiana

Titel

Acute Exposure to Low Lead Levels and its Implications on the Activity and Expression of Cytosolic Thioredoxin Reductase in the Kidney

Ist Teil von

• Basic & clinical pharmacology & toxicology, 2014-06, Vol.114 (6), p.476-484

Ort / Verlag

Oxford: Blackwell

Erscheinungsjahr

2014

Quelle

Wiley Online Library All Journals

Beschreibungen/Notizen

• Renal thioredoxin reductase‐1 (TrxR‐1) activity is stimulated at lead doses lower than that necessary to inhibit δ‐aminolevulinate dehydratase activity (δ‐ALA‐D), which is a classical early biomarker of lead effects. Thus, we hypothesized that the activity of TrxR‐1 could be a more sensitive early indicator of lead effects than is δ‐ALA‐D. To evaluate this hypothesis, we assessed the blood and renal TrxR‐1 activity and its gene expression along with biomarkers of oxidative damage, antioxidant enzyme activities and biomarkers of lead exposure in rats acutely exposed to lead. A histopathological analysis was performed to verify renal damage. The increase in renal TrxR‐1 activity paralleled the increase in the blood and renal lead levels at 6, 24 and 48 hr after the exposure to 25 mg/kg lead acetate (p < 0.05), whereas its expression was increased 24 and 48 hr after exposure. These effects were not accompanied by oxidative or tissue damage in the kidneys. Blood TrxR‐1 activity was not affected by lead exposure (up to 25 mg/kg). Erythrocyte δ‐ALA‐D activity was inhibited 6 hr after the exposure to 25 mg/kg lead acetate (p < 0.05) but recovered thereafter. Renal δ‐ALA‐D activity decreased 24 and 48 hr after the exposure to 25 mg/kg lead acetate. There were no changes in any parameters at lead acetate doses <25 mg/kg. Our results indicate that blood TrxR‐1 activity is not a suitable indicator of lead effects. In contrast, the increase in renal TrxR‐1 expression and activity is implicated in the early events of lead exposure, most likely as a protective cellular mechanism against lead toxicity.