Alteration in thiols homeostasis, protein and lipid peroxidation in renal tissue following subacute oral exposure of imidacloprid and arsenic in Wistar rats

被引:23
作者
Mahajan, Lakshay [1 ]
Verma, Pawan Kumar [1 ]
Raina, Rajinder [1 ]
Pankaj, Nrip K. [1 ]
Sood, Shilpa [2 ]
Singh, Maninder [3 ]
机构
[1] Sher E Kashmir Univ Agr Sci & Technol Jammu, Fac Vet Sci & Anim Husb, Div Vet Pharmacol & Toxicol, Rs Pura 181102, India
[2] Sher E Kashmir Univ Agr Sci & Technol Jammu, Fac Vet Sci & Anim Husb, Div Vet Pathol, Rs Pura 181102, India
[3] Sher E Kashmir Univ Agr Sci & Technol Jammu, Fac Vet Sci & Anim Husb, Div Vet Publ Hlth & Epidemiol, Rs Pura 181102, India
关键词
Imidacloprid; Arsenic; Malondialdehyde; Nephrotoxicity; Thiols;
D O I
10.1016/j.toxrep.2018.11.003
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
The aim of present study was to assess whether No Observed Effect Level (NOEL) of imidacloprid (IMI) potentiates the arsenic induced renal toxicity at its maximum contaminant level in drinking water in Wistar rats. Significant elevation of lipid and protein oxidation with reduced level of total thiols and antioxidant enzymes (catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione-s-transferase) in renal tissue may have contributed to increased renal plasma biomarkers (creatinine and blood urea nitrogen) following repeated exposure of IMI and arsenic alone and in-combination. The altered renal biomarkers in co-exposed groups corroborated with histopathological alterations in renal tissue. The observations indicated that altered thiol homeostasis in renal tissue may be associated with increased lipid and protein oxidation in IMI and arsenic administered rats. It is concluded that administration of IMI potentiate the arsenic induced renal damage in Wistar rats.
引用
收藏
页码:1114 / 1119
页数:6
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