TY - JOUR
T1 - Acute effects of diesel exhaust particles and cisplatin on oxidative stress in cultured human kidney (HEK 293) cells, and the influence of curcumin thereon
AU - Waly, Mostafa I.
AU - Ali, Badreldin H.
AU - Nemmar, Abderrahim
N1 - Funding Information:
This work was supported by a SQU-UAEU joint grant provided to both Prof. B.H. Ali (SQU) and Prof. A. Nemmar (UAEU), and by a research grant from the College of Agricultural and Marine Sciences, SQU (IG/AGR/FOOD/10/01). The help of Professor Richard Deth, Northeastern University, Boston, USA, in the cysteine uptake measurements is acknowledged.
PY - 2013/12
Y1 - 2013/12
N2 - Particulate air pollution with particle diameters less than 2.5. μm contribute to respiratory and extra-respiratory morbidity and mortality. We have recently reported the first in vivo experimental evidence that Diesel exhaust particles (DEP) in the lung aggravated the renal, pulmonary, and systemic effects of cisplatin (CP)-induced acute renal failure in rats. This in vitro study sought to determine whether and to what extent does DEP exposure exacerbate the effects of CP-induced oxidative stress in human embryonic kidney (HEK-293) cells, and to examine if these effects could be mitigated/prevented with curcumin (the yellow pigment isolated from turmeric). Cells viability, cysteine uptake and oxidative stress indices [glutathione (GSH), total antioxidant capacity (TAC), and the activities of antioxidant enzymes (catalase; glutathione peroxidase; superoxide dismutase)] were evaluated in all study groups. DEP aggravated the CP- induced HEK-293 cells toxicity, as evidenced by decreasing cell viability and by inducing oxidative stress (GSH depletion, TAC impairment, and antioxidant enzymes inhibition). DEP, but not CP, significantly reduced cysteine uptake. Curcumin prevented the observed DEP and CP-induced cellular insults. These findings suggest that DEP augmented the CP-induced toxicity in HEK-293 cells. Curcumin exhibited a strong potential for protection against DEP and CP-induced cytotoxicity.
AB - Particulate air pollution with particle diameters less than 2.5. μm contribute to respiratory and extra-respiratory morbidity and mortality. We have recently reported the first in vivo experimental evidence that Diesel exhaust particles (DEP) in the lung aggravated the renal, pulmonary, and systemic effects of cisplatin (CP)-induced acute renal failure in rats. This in vitro study sought to determine whether and to what extent does DEP exposure exacerbate the effects of CP-induced oxidative stress in human embryonic kidney (HEK-293) cells, and to examine if these effects could be mitigated/prevented with curcumin (the yellow pigment isolated from turmeric). Cells viability, cysteine uptake and oxidative stress indices [glutathione (GSH), total antioxidant capacity (TAC), and the activities of antioxidant enzymes (catalase; glutathione peroxidase; superoxide dismutase)] were evaluated in all study groups. DEP aggravated the CP- induced HEK-293 cells toxicity, as evidenced by decreasing cell viability and by inducing oxidative stress (GSH depletion, TAC impairment, and antioxidant enzymes inhibition). DEP, but not CP, significantly reduced cysteine uptake. Curcumin prevented the observed DEP and CP-induced cellular insults. These findings suggest that DEP augmented the CP-induced toxicity in HEK-293 cells. Curcumin exhibited a strong potential for protection against DEP and CP-induced cytotoxicity.
KW - Cisplatin
KW - Cultured kidney cells
KW - Curcumin
KW - Diesel exhaust particles
KW - Oxidative stress
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U2 - 10.1016/j.tiv.2013.09.023
DO - 10.1016/j.tiv.2013.09.023
M3 - Article
C2 - 24113306
AN - SCOPUS:84886838735
SN - 0887-2333
VL - 27
SP - 2299
EP - 2304
JO - Toxicology in Vitro
JF - Toxicology in Vitro
IS - 8
ER -