Potential role of N-acetylcysteine on chlorpyrifos-induced neurotoxicity in rats
In: Environmental science and pollution research: ESPR, Band 26, Heft 20, S. 20731-20741
ISSN: 1614-7499
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In: Environmental science and pollution research: ESPR, Band 26, Heft 20, S. 20731-20741
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 27, Heft 12, S. 13237-13246
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 30, Heft 9, S. 23237-23247
ISSN: 1614-7499
Abstract
Many studies have reported that cadmium (Cd) can induce liver cell injury; however, the toxicity mechanisms of Cd on the liver have not been fully explained. Thirty-two male albino rats were divided into four groups: the control group, the N-acetylcysteine (NAC) group orally as effervescent instant sachets with a concentration of 200 mg dissolved in distilled water and dosage was 200 mg/kg body weight freshly prepared, the cadmium chloride (CdCl2) group (treated with 3 mg/kg orally), and the N-acetylcysteine (NAC) + cadmium chloride group (treated with 200 mg/kg orally post to CdCl2) for 60 days. The NAC alone did not make notable changes in most of the parameters. The CdCl2 alone, compared to control, induced significant alterations in oxidative stress markers (increment in lipid peroxidation (LPO) and nitric oxide (NO)) and antioxidant defense system (decrement in superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx)), which resulted in a downregulation of pro-apoptotic Bcl2-associated X protein (Bax) and caspase-3 and upregulation of anti-apoptotic B-cell leukemia/lymphoma 2 (Bcl2) protein as well as the survival fate of hepatic cells. Post-administration of NAC to CdCl2 resulted in a reduction in oxidative stress markers, shifting of cells from the G2/M phase to the G0/G1 inhibiting signal-regulated kinase activation, and impairment of the anti-apoptotic signaling pathway when compared to the CdCl2 group alone. Accordingly, the Bcl2/Bax ratio was reduced to 1.17-fold change, as an adaptive process to hepatic tissue injury. These findings demonstrated that NAC would attenuate the possibility of oxidative stress and cytotoxicity of hepatic tissue induced by CdCl2.
In: Environmental science and pollution research: ESPR, Band 28, Heft 14, S. 17482-17494
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 27, Heft 14, S. 17184-17193
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 30, Heft 24, S. 65822-65834
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 29, Heft 8, S. 12300-12312
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 27, Heft 11, S. 12395-12404
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 27, Heft 4, S. 3979-3991
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 29, Heft 31, S. 47539-47548
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 26, Heft 13, S. 13539-13550
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 27, Heft 6, S. 5981-5992
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 27, Heft 3, S. 3401-3412
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 29, Heft 55, S. 83723-83732
ISSN: 1614-7499
In: Environmental science and pollution research: ESPR, Band 28, Heft 29, S. 39625-39636
ISSN: 1614-7499