Diethylnitrosamine aggravates cadmium-induced hepatorenal oxidative damage in prepubertal rats

Abstract

The adverse health consequences of environmental, occupational, and dietary exposure to either diethylnitrosamine (DEN) or cadmium (Cd) have been widely investigated. However, because most environmental exposures to xenobiotics do not occur in isolation but in mixtures, the effects of simultaneous exposure to both DEN and Cd on hepatorenal function deserves investigation. The present study investigated the impact of 7 days oral co-exposure to 10 mg/kg body weight (b.w.) of DEN and 5 mg/kg b.w. of Cd on biomarkers of hepatic and renal functions, antioxidant defense systems, and oxidative stress indices in the liver and kidney of prepubertal rats. The results showed that the significant ( p < 0.05) increases in the levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, gamma glutamyl transferase, urea, and creatinine following separate administration of DEN and Cd to rats were further increased in the co-exposure group. Moreover, marked decreases in the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase as well as glutathione levels following individual administration of DEN and Cd to rats were exacerbated in the co-exposure group. Further, the marked increase in the lipid peroxidation level and the histopathological lesions in the liver and kidney of rats treated with DEN or Cd alone were intensified in the co-exposure group These findings indicate that co-exposure to DEN and Cd elicited more severe hepatic and renal oxidative damage in the rats, thus suggesting a greater risk to humans who are co-exposed to them.

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“…Oxidative injury has a key role in mediating the hepatic and renal detrimental effects of Cd [ 11 , 48 ]. Cd-intoxicated rats exhibited a disturbance in the oxidant/antioxidant status.…”

Protective effect of quercetin on cadmium-induced renal apoptosis through cyt-c/caspase-9/caspase-3 signaling pathway

“…Histopathological changes could directly reflect the damage to kidney tissue. Cd caused significant histomorphological changes in the kidney, a similar phenomenon was also observed by Owumi et al ( Owumi et al, 2019 ). It is speculated that it may be related to the excessive accumulation of free radicals in the body caused by Cd exposure ( Jihen el et al, 2009 ).…”

“…GSH levels in Cd-treated rats were greater than in control rats in the current study. However, some reports indicated that Cd exposure significantly reduced GSH levels, which is inconsistent with some research findings (Jihen el et al, 2010;Renugadevi and Prabu, 2010;Owumi et al, 2019). The reason may be that after Cd enters the body, in order to resist the oxidative damage caused by stress, a large amount of GSH is produced in the body through chelation to remove free Cd 2+ .…”

N ‐acetyl cysteine co‐treatment abates perfluorooctanoic acid‐induced reproductive toxicity in male rats

“…Glutathione‐s‐transferase (GST) activity was determined using the previously reported method of Habig (Habig et al., 1974; Owumi, et al., 2019) using 1‐chloro‐2,4‐dinitrobenzene (CDNB) as a substrate. G S T is extremely activity with the substrate 1‐chloro‐2,4‐dinitrobenzene.…”