TY  - JOUR
AB  - Cardiovascular disease (CVD) is a broad term that incorporated a group of conditions that affect the blood vessels and the heart. CVD is a foremost cause of fatalities around the world. Multiple pathophysiological mechanisms are involved in CVD; however, oxidative stress plays a vital role in generating reactive oxygen species (ROS). Oxidative stress occurs when the concentration of oxidants exceeds the potency of antioxidants within the body while producing reactive nitrogen species (RNS). ROS generated by oxidative stress disrupts cell signaling, DNA damage, lipids, and proteins, thereby resulting in inflammation and apoptosis. Mitochondria is the primary source of ROS production within cells. Increased ROS production reduces nitric oxide (NO) bioavailability, which elevates vasoconstriction within the arteries and contributes to the development of hypertension. ROS production has also been linked to the development of atherosclerotic plaque. Antioxidants can decrease oxidative stress in the body; however, various therapeutic drugs have been designed to treat oxidative stress damage due to CVD. The present review provides a detailed narrative of the oxidative stress and ROS generation with a primary focus on the oxidative stress biomarker and its association with CVD. We have also discussed the complex relationship between inflammation and endothelial dysfunction in CVD as well as oxidative stress-induced obesity in CVD. Finally, we discussed the role of antioxidants in reducing oxidative stress in CVD.
AU  - Panda, P.*
AU  - Verma, H.K.
AU  - Lakkakula, S.*
AU  - Merchant, N.*
AU  - Kadir, F.*
AU  - Rahman, S.*
AU  - Jeffree, M.S.*
AU  - Lakkakula, B.V.K.S.*
AU  - Rao, P.V.*
C1  - 65625
C2  - 52748
TI  - Biomarkers of oxidative stress tethered to cardiovascular diseases.
JO  - Oxid. Med. Cell. Longev.
VL  - 2022
PY  - 2022
SN  - 1942-0900
ER  - 

TY  - JOUR
AB  - BACKGROUND: Reactive oxygen species- (ROS-) mediated ischemia-reperfusion injury (IRI) detrimentally impacts liver transplantation and resection. 12/15-Lipoxygenase (12/15-LOX), an antagonistic protein of the glutathione peroxidase 4 (GPX4) signaling cascade, was proven to mediate cell death in postischemic cerebral and myocardial tissue. The aim of this study was to investigate the impact of 12/15-LOX inhibition on hepatic IRI. METHODS: Livers of C57BL/6 mice were exposed to 60 minutes of partial warm ischemia and 90 minutes of reperfusion after previous Baicalein administration, an inhibitor of 12/15-LOX. Tissue samples were analyzed by TUNEL assay, Western blot, and spectral photometry. RESULTS: TUNEL labeling showed a significant reduction of hepatic cell death following baicalein pretreatment. Western Blot analysis revealed a significant downregulation of Jun-amino-terminal-kinase (JNK), caspase-3, and poly-ADP-ribose-polymerase (PARP), besides considerably lowered p44/42-MAP-kinase (ERK1/2) expression after Baicalein administration. A significant elevation of glutathione oxidation was measured in Baicalein pretreated livers. CONCLUSION: Our data show that inhibition of 12/15-lipoxygenase causes significant cell death reduction after hepatic ischemia and reperfusion by enhancing glutathione metabolism. We conclude that GPX4-dependent cell death signaling cascade might play a major role in development of hepatic IRI, in which the investigated proteins JNK, caspase-3, ERK1/2, and PARP might contribute to tissue damage.
AU  - Drefs, M.*
AU  - Thomas, M.N.*
AU  - Guba, M.*
AU  - Angele, M.K.*
AU  - Werner, J.*
AU  - Conrad, M.
AU  - Steib, C.J.*
AU  - Holdt, L.M.*
AU  - Andrassy, J.*
AU  - Khandoga, A.*
AU  - Rentsch, M.*
C1  - 51722
C2  - 43466
CY  - London
TI  - Modulation of glutathione hemostasis by inhibition of 12/15-lipoxygenase prevents ROS-mediated cell death after hepatic ischemia and reperfusion.
JO  - Oxid. Med. Cell. Longev.
VL  - 2017
PB  - Hindawi Ltd
PY  - 2017
SN  - 1942-0900
ER  - 

TY  - JOUR
AB  - Vertebrate respiratory chain complex III consists of eleven subunits. Mutations in five subunits either mitochondrial (MT-CYB) or nuclear (CYC1, UQCRC2, UQCRB, and UQCRQ) encoded have been reported. Defects in five further factors for assembly (TTC19, UQCC2, and UQCC3) or iron-sulphur cluster loading (BCS1L and LYRM7) cause complex III deficiency. Here, we report a second patient with UQCC2 deficiency. This girl was born prematurely; pregnancy was complicated by intrauterine growth retardation and oligohydramnios. She presented with respiratory distress syndrome, developed epileptic seizures progressing to status epilepticus, and died at day 33. She had profound lactic acidosis and elevated urinary pyruvate. Exome sequencing revealed two homozygous missense variants in UQCC2, leading to a severe reduction of UQCC2 protein. Deficiency of complexes I and III was found enzymatically and on the protein level. A review of the literature on genetically distinct complex III defects revealed that, except TTC19 deficiency, the biochemical pattern was very often a combined respiratory chain deficiency. Besides complex III, typically, complex I was decreased, in some cases complex IV. In accordance with previous observations, the presence of assembled complex III is required for the stability or assembly of complexes I and IV, which might be related to respirasome/supercomplex formation.
AU  - Feichtinger, R.G.*
AU  - Brunner-Krainz, M.*
AU  - Alhaddad, B.*
AU  - Wortmann, S.B.
AU  - Kovács-Nagy, R.*
AU  - Stojakovic, T.*
AU  - Erwa, W.*
AU  - Resch, B.*
AU  - Windischhofer, W.*
AU  - Verheyen, S.*
AU  - Uhrig, S.*
AU  - Windpassinger, C.*
AU  - Locker, F.*
AU  - Makowski, C.*
AU  - Strom, T.M.
AU  - Meitinger, T.
AU  - Prokisch, H.
AU  - Sperl, W.*
AU  - Haack, T.B.
AU  - Mayr, J.A.*
C1  - 51728
C2  - 43380
CY  - London
TI  - Combined respiratory chain deficiency and UQCC2 mutations in neonatal encephalomyopathy: Defective supercomplex assembly in complex III deficiencies.
JO  - Oxid. Med. Cell. Longev.
VL  - 2017
PB  - Hindawi Ltd
PY  - 2017
SN  - 1942-0900
ER  -