ubiquinone/necrosis

It has been shown that prophylactic administration of ubiquinone protects rats liver from the toxic damage by D-galactosamine both on ultrastructural and on cell levels. Ubiquinone administration prevents necrosis in hepatocytes and preserves their ability for compensatory reactions expressed in

Nitric oxide (NO) is an important signal substance in cell-cell communication and can induce relaxation of blood vessels by activating guanylate cyclase in smooth muscle cells (SMCs). NO is synthesized from L-arginine by the enzyme NO synthase, which is present in endothelial cells. It was recently

Over doses of Paracetamol (panadol; acetaminophen) can cause life-threatening renal damage. This study compared the impact of nano-ubiquinone (Nubiq) with native ubiquinone (ubiq) reducing damage induced by Paracetamol-toxicity in rats. Paracetamol treatment produced an elevation in serum urea, uric

The effects of ubiquinone 50 (synthetic coenzyme Q10) and viral infection on phytohemagglutinin activity were studied in the tobacco (Nicotiana tabacum L.) cultivar Samsun NN, which carries the necrosis-formation locus and exhibits hypersensitivity to tobacco mosaic virus (TMV) and ubiquinone (Q10).

As a class, hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors can potentially cause skeletal myopathy. One statin, cerivastatin, has recently been withdrawn from the market due to an unacceptably high incidence of rhabdomyolysis. The mechanism underlying statin-induced myopathy is

Tumor necrosis factor (TNF)-alpha increases mitochondrial reactive oxygen species (ROS) production in tumor cells and hepatocytes. However, whether TNF-alpha stimulates mitochondrial ROS production in endothelial cells (EC) has not yet been reported. We studied the effect of TNF-alpha on

Structural mitochondrial damage accompanies the cytotoxic effects of several drugs including tumor necrosis factor (TNF). Using various inhibitors of mitochondrial electron transport we have investigated the mechanism of TNF-mediated cytotoxicity in L929 and WEHI 164 clone 13 mouse fibrosarcoma

With the recognition of the central role of mitochondria in apoptosis, there is a need to develop specific tools to manipulate mitochondrial function within cells. Here we report on the development of a novel antioxidant that selectively blocks mitochondrial oxidative damage, enabling the roles of

OBJECTIVE To study whether CO-Q10 can protect liver injury caused by acute on chronic liver failure (ACLF) by autophagy. METHODS Rats were separated into three groups: control group, acute on chronic liver failure (ACLF) and intervenient group, liver tissues were observed by optical microscopy and

BACKGROUND In this study, the effect of coenzyme Q10 (CQ10) on flap survival was investigated. METHODS Fifty Wistar Albino rats were divided into 5 groups. The survival rates of the skin flaps were assessed 10 days after complete elevation of the flaps. Regions of survival and necrosis were drawn on

Ubiquinol is the two-electron reduction product of ubiquinone (coenzyme Q(10) or CoQ(10)) and functions as an antioxidant in both mitochondria and lipid membranes. In humans and most mammals, including dogs, the predominant form of coenzyme Q is coenzyme Q(10), whereas the primary form in rodents is

Although nitric oxide (.N = O) biosynthesis is inducible in rat hepatocytes (HC), the physiological significance of .N = O production by these cells is unknown. Short exposure of HC to authentic .N = O led to a concentration-dependent inhibition of mitochondrial aconitase, NADH-ubiquinone

OBJECTIVE There is a growing body of evidence to suggest that low-density lipoprotein (LDL) cholesterol, inflammation and oxidative stress are pivotal in the development of cardiovascular disease, but their interconnections are not well known. The objective of this study was to determine whether

A male infant with glutaric aciduria II secondary to electron transfer flavoprotein: ubiquinone oxidoreductase deficiency is compared to previously reported cases of glutaric aciduria II. A common pattern of anomalies in patients with malformations (8/16) includes macrocephaly, large anterior

OBJECTIVE To investigate the morphology alterations and proteomics changes in primary astrocytes following fluid percussion injury. METHODS Primary cultures of astrocytes were prepared from cerebral hemispheres of 1-3 d-old SD rats, then, astrocytes were randomly divided into control group and