Home CONTACT General Physiology and Biophysics 2017 General Physiology and Biophysics Vol.36, No.3, p.309–320, 2017

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.36, No.3, p.309–320, 2017

Title: Involvement of oxidative stress in the mechanism of p,p’-DDT-induced nephrotoxicity in adult rats
Author: Neila Marouani, Dorsaf Hallegue, Mohsen Sakly, Moncef Benkhalifa, Khémais Ben Rhouma, Olfa Tebourbi

Abstract: The 1,1,1-trichloro-2,2-bis(4-chlorophenyl) ethane (p,p’-DDT) is an organochlorine pesticide that persists in the environment and has a risk to human health. We investigated whether p,p’-DDT-induces nephrotoxicity in rats and whether oxidative stress and apoptosis are involved in the pathogenesis of this process. Male rats received the pesticide at doses of 50 and 100 mg/kg for 10 days. Renal damage was evaluated by histopathological examination and serum markers. The oxidative stress was evaluated by lipid peroxidation (LPO), metallothioneins (MTs) and protein carbonyl levels. Antioxidant enzymes were assessed by determination of superoxide dismutase (SOD) and catalase (CAT) activities. Glutathione-dependent enzymes and reducing power in kidney were evaluated by glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST) activities. Renal tubular cells apoptosis was assessed through the TUNEL assay. After 10 days of treatment, an increase of serum creatinine and urea levels occurred, LPO and protein carbonyl levels were increased, while MTs level, SOD and CAT activities were decreased. Besides, the GPx, GR, GST, and GSH activities were decreased. Histological alterations in kidney tissue and intense apoptosis in renal tubular cells were observed. These results suggest that DDT sub-acute treatment causes oxidative stress and apoptosis, which may be the chief mechanisms of DDT-induced nephrotoxicity.

Keywords: Apoptosis — Histopathology — Kidney — Oxidative stress — p,p’-DDT — Rat
Published online: 01-Jun-2017
Year: 2017, Volume: 36, Issue: 3 Page From: 309, Page To: 320
doi:10.4149/gpb_2016050


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