coenzyme-q10 and Necrosis

Sepsis is one of the main causes of death among critically ill patients. Sepsis pathogenesis includes infection by gram-negative and gram-positive bacteria, fungi, or both; exacerbated inflammatory response; hypotension, with potential to cause vasodilatory shock; and lesser delivery of oxygen to tissues due to impairment of oxygen utilization by cells. The participation of reactive species and/or free radicals such as nitric oxide (NO), peroxynitrite (ONOO

Topics: Adenosine Triphosphate; Animals; Antioxidants; Apoptosis; Humans; Melatonin; Mitochondria; Multiple Organ Failure; Necrosis; NF-kappa B; Organophosphorus Compounds; Oxidative Stress; Selenium; Sepsis; Ubiquinone; Vitamins

Coenzyme Q10 (CoQ10) which acts as an electron transporter in the mitochondrial respiratory chain has many beneficial effects on liver diseases. In our previous research, CoQ10 has been found to attenuate acetaminophen (APAP)-induced acute liver injury (ALI). However, whether CoQ10 administration is still effective at the late stage of APAP overdose is still unknown. In this study, we aimed to test CoQ10 efficacy at the late stage of APAP overdose. C57BL/6J mice were intraperitoneally treated with APAP to induce liver injury. CoQ10 (5 mg/kg) was given to mice at 16 h after APAP treatment. The results showed that while CoQ10 treatment at 16 h post-APAP overdose had no effects on the expression of ROS generated genes or scavenged genes, it still significantly decreased necrosis of hepatocytes following APAP-induced ALI. Moreover, CoQ10 increased MerTK+ macrophages accumulation in the APAP-overdose liver and inhibition of MerTK signaling partly abrogated the protective role of CoQ10 treatment on the hepatic necrosis. CoQ10 treatment also significantly enhanced hepatocytes proliferation as shown in the increased 5-bromodeoxyuridine incorporation in the APAP-intoxicated mice liver section. In addition, CoQ10 treatment increased hepatic Proliferating Cell Nuclear Antigen (PCNA) and Cyclin D1 expression and promoted activation of the β-catenin signaling in APAP-overdose mice. To conclude, these data provide evidence that CoQ10 treatment is still effective at the late stage of APAP-induced ALI and promotes resolution of necrosis and liver regeneration following ALI.

Topics: Acetaminophen; Animals; Chemical and Drug Induced Liver Injury; Chemical and Drug Induced Liver Injury, Chronic; Hepatocytes; Liver; Liver Regeneration; Mice; Mice, Inbred C57BL; Necrosis; Ubiquinone

Doxorubicin (DXR) extravasation result with serious morbidity like skin ulceration and necrosis. The purpose of this study is to determine the protective effects of ozone, olive oil, dimethyl sulfoxide (DMSO), and coenzyme Q10 in the treatment of DXR-induced skin ulcers on rats. After an intradermal injection of DXR on a basis of an animal extravasation model, the materials were topically applied. The ulcer sizes were measured, and a punch biopsy was taken from the extravasation site in which the skin ulcers formed at the end of the experiment. The samples were analyzed for tumor necrosis factor alpha (TNF-α), interleukin 1-beta (IL1β), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) enzymes, and examined histopathologically. The ulcer sizes clearly decreased in the study groups, including DMSO, olive oil, ozone plus coenzyme Q10, and ozone plus olive oil groups in comparison with the control group with the exception of the coenzyme Q10 group. The malondialdehyde levels were lower in the DMSO, olive oil, ozone plus olive oil, and ozone plus coenzyme Q10 groups than they were in the control group, but they were not significantly different. The TNF-α level was lower in the DMSO, ozone plus olive oil, coenzyme Q10, and ozone plus coenzyme Q10 groups in comparison with the control group. There was no significant change in the SOD, GSH-Px, and IL1β levels in the study groups in comparison with the control and the sham groups. The ozone plus olive oil group could be considered to be an alternate therapy for skin ulcers due to DXR extravasation.

Topics: Animals; Antibiotics, Antineoplastic; Antioxidants; Biopsy; Dimethyl Sulfoxide; Disease Models, Animal; Doxorubicin; Extravasation of Diagnostic and Therapeutic Materials; Necrosis; Olive Oil; Oxidative Stress; Ozone; Rats; Skin; Skin Ulcer; Ubiquinone

Autologous fat is an attractive soft-tissue filler in plastic and reconstructive surgery. The success of the procedure relies strongly on the technique of transferring viable preadipocytes. Among other factors, preadipocyte viability is impaired by local anesthetics. Application of coenzyme Q10 is being performed by aesthetic plastic surgeons to enhance the success of lipotransfer. The aim of this study was to evaluate the effect of Q10 on preadipocyte viability with special regard to impairment after lidocaine treatment.. Preadipocytes were pretreated with coenzyme Q10 or vehicle control followed by incubation with lidocaine for 30 min. Viability and apoptosis were assessed by FACS analysis and Western blot.. Coenzyme Q10 did not improve viability nor have any effect on investigated apoptosis parameters. Preadipocyte viability was reduced after lidocaine treatment. Surface binding of annexin V, cleavage of caspase-3, and abundance of subdiploid cells were not detectable though, suggesting that necrosis rather than apoptosis is the cause for reduced preadipocyte viability.. Our results indicate that Q10 does not improve preadipocyte viability. Preadipocyte cell death induced by lidocaine is not caused by apoptosis but by necrosis, which cannot be prevented by coenzyme Q10. These findings should be taken into account when searching for solutions to improve preadipocyte viability in the context of soft tissue engineering and autologous fat transfer.

Topics: Adipocytes; Adipose Tissue; Anesthetics, Local; Apoptosis; Cell Survival; Humans; Lidocaine; Necrosis; Transplantation, Autologous; Ubiquinone

The aim of the study was to observe the effect of coenzyme Q10 and vitamin E supplementation on the course of the regeneration process of the longissimus lumborum muscle after bupivacaine-induced myonecrosis as well as to determine the correlation between the level of those substances in plasma and their levels in damaged and non-damaged muscular tissue in pigs. The obtained results indicate that the course of regeneration of a damaged muscle is affected to a higher extent by coenzyme Q10 than by vitamin E. The administration of coenzyme Q10 and vitamin E has a significant impact on the increase in the level of those substances in damaged muscles and plasma of animals.

Topics: Anesthetics, Local; Animal Feed; Animals; Antioxidants; Bupivacaine; Coenzymes; Female; Muscle, Skeletal; Muscular Diseases; Necrosis; Regeneration; Swine; Swine Diseases; Ubiquinone; Vitamin E

Topics: Allopurinol; Animals; Aspartate Aminotransferases; Coenzymes; Dose-Response Relationship, Drug; Free Radicals; Glutathione; Liver; Necrosis; Oxygen; Rats; Rats, Inbred Lew; Reperfusion Injury; Superoxide Dismutase; Temperature; Ubiquinone

Topics: Animals; Cardiomyopathies; Coenzymes; Female; Isoproterenol; Male; Mitochondria, Heart; Myocardium; Necrosis; Rats; Ubiquinone