• Environmental Analysis Health and Toxicology
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• v.29
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• pp.1.1-1.7
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• 2014

Objectives The present subacute study was designed to evaluate the effect of coenzyme Q 10 (CoQ10) in the 28 days aroclor 1254 exposure induced oxidative stress in mice brain. Methods Biochemical estimations of brain lipid peroxidation (LPO), reduced glutathione (GSH), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and acetyl cholinesterase (AChE), and histopathological investigations of brain tissue were carried out. Results Oral exposure of aroclor 1254 (5 mg/kg) led to significant decrease in levels of GSH, and activities of SOD, CAT, GPx, and AChE, and increase in LPO. These aberrations were restored by CoQ10 (10 mg/kg, intraperitoneal injection [IP]). This protection offered was comparable to that of L-deprenyl (1 mg/kg, IP) which served as a reference standard. Conclusions Aroclor 1254 exposure hampers the activities of various antioxidant enzymes and induces oxidative stress in the brains of Swiss albino mice. Supplementation of CoQ10 abrogates these deleterious effects of aroclor 1254. CoQ10 also apparently enhanced acetyl cholinesterase activity which reflects its influence on the cholinergic system.

• The Korean Journal of Mycology
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• v.28 no.1
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• pp.55-59
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• 2000

This study was carried out to investigate the antioxidative and chemopreventive effects of the extracts from Polyozellus multiplex, an edible mushroom through in vitro and in vivo assay. Polyozellus multiplex fractions were assayed for its antioxidative effect with colony formation assay. Polyozellus multiplex methanol extract and water fraction showed protective effects against the cytotoxicity of $H_2O_2$. The modifying effects of Polyozellus multiplex methanol extract and water fraction on the induction of carcinogenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were investigated in Wistar rats. The GSH content was decreased by MNNG treatment but was increased by adding Polyozellus multiplex water fractions. Also the activity of glutathione S-transferase and the superoxide dismutase levels were increased by the treatment of Polyozellus multiplex water fractions more than with MNNG alone. In addition to the Polyozellus multiplex water fraction increased the p53 expression as compared with the value of MNNG alone.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.5
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• pp.411-418
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• 2014

Vascular remodelling is an adaptive mechanism, which counteracts pressure changes in blood circulation. Nicotine content in cigarette increases the risk of hypertension. The exact relationship between nicotine and vascular remodelling still remain unknown. Current study was aimed to determine the effect of clinically relevant dosage of nicotine (equivalent to light smoker) on aortic reactivity, oxidative stress markers and histomorphological changes. Twelve age-matched male Sprague-Dawley rats were randomly divided into two groups, i.e.: normal saline as control or 0.6 mg/kg nicotine for 28 days (i.p., n=6 per group). On day-29, the rats were sacrificed and the thoracic aorta was dissected immediately for further studies. Mean arterial pressure (MAP) and pulse pressure (PP) of nicotine-treated vs. control were significantly increased (p<0.05). Nicotine-treated group showed significant (p<0.05) increase tunica media thickness, and decrease in lumen diameter, suggesting vascular remodelling which lead to prior hypertension state. The phenylephrine (PE)-induced contractile response in nicotine group was significantly higher than control group ($ED_{50}=1.44{\times}10^5M$ vs. $4.9{\times}10^6M$) (p<0.05~0.001). However, nicotine-treated rat showed significantly lower endothelium-dependent relaxation response to acetylcholine (ACh) than in control group ($ED_{50}=6.17{\times}10^7M$ vs. $2.82{\times}10^7M$) (p<0.05), indicating loss of primary vascular function. Malondialdehyde (MDA), a lipid peroxidation marker was significantly higher in nicotine group. Superoxide dismutase (SOD) enzymatic activity and glutathione (GSH) were all reduced in nicotine group (p<0.05) vs. control, suggesting nicotine induces oxidative imbalance. In short, chronic nicotine administration impaired aortic reactivity, probably via redox imbalance and vascular remodelling mechanism.