Reactive oxygen species (ROS) generated after exposure to ionizing radiation and toxic peptides, in mitochondrial metabolism and during aging contribute to damage of cell&#x2019;s structural and functional components and can lead to diseases. Monomers and small oligomers of amyloid beta (A&#x03B2;) peptide, players in Alzheimer&#x2019;s disease, are recently suggested to be involved in damaging of neurons, instead of extracellular A&#x03B2; plaques. We demonstrate that externally applied disaggregated A&#x03B2;1&#x2013;42 peptide interacts preferentially with acidic compartments (lysosomes). We compared standard cell cultivation (21&#x0025; O2) to more physiological cell cultivation (5&#x0025; O2). Cells did not exhibit a dramatic increase in ROS and change in glutathione level upon 4&#x2009;&#x03BC;M A&#x03B2; peptide treatment, whereas exposure to 2&#x2009;Gy X-rays increased ROS and changed glutathione level and ATP concentration. The occurrence of the 4977&#x2009;bp deletion in mtDNA and significant protein carbonylation were specific effects of IR and more pronounced at 21&#x0025; O2. An increase in cell death after A&#x03B2; peptide treatment or irradiation was unexpectedly restored to the control level or below when both were combined, particularly at 5&#x0025; O2. Therefore, A&#x03B2; peptide at low concentration can trigger neuroprotective mechanisms in cells exposed to radiation. Oxygen concentration is an important modulator of cellular responses to stress.

Tamara D&#x017E;ini&#x0107;

Norbert A. Dencher

Oxygen Concentration and Oxidative Stress Modulate the Influence of Alzheimer&#x2019;s Disease A&#x03B2;1&#x2013;42 Peptide on Human Cells

Alterations in cardiac energy metabolism play a key role in the pathogenesis of diabetic cardiomyopathy. Hypercholesterolemia associated with bioenergetic impairment and oxidative stress has not been well characterized in the cardiac function under glycemic control deficiency conditions. This work aimed to determine the cardioprotective effects of quercetin (QUE) against the damage induced by a high-cholesterol (HC) diet in hyperglycemic rats, addressing intracellular antioxidant mechanisms and bioenergetics. Quercetin reduced HC-induced alterations in the lipid profile and glycemia in rats. In addition, QUE attenuated cardiac diastolic dysfunction (increased E:A ratio), prevented cardiac cholesterol accumulation, and reduced the increase in HC-induced myocyte density. Moreover, QUE reduced HC-induced oxidative stress by preventing the decrease in GSH/GSSG ratio, Nrf2 nuclear translocation, HO-1 expression, and antioxidant enzymatic activity. Quercetin also counteracted HC-induced bioenergetic impairment, preventing a reduction in ATP levels and alterations in PGC-1&#x03B1;, UCP2, and PPAR&#x03B3; expression. In conclusion, the mechanisms that support the cardioprotective effect of QUE in rats with HC might be mediated by the upregulation of antioxidant mechanisms and improved bioenergetics on the heart. Targeting bioenergetics with QUE can be used as a pharmacological approach to modulate structural and functional changes of the heart under hypercholesterolemic and hyperglycemic conditions.

Rodrigo L. Castillo

Emilio A. Herrera

Alejandro Gonzalez-Candia

Marjorie Reyes-Farias

Nicole de la Jara

Juan Pedro Pe&#x00F1;a

Catalina Carrasco-Pozo

Quercetin Prevents Diastolic Dysfunction Induced by a High-Cholesterol Diet: Role of Oxidative Stress and Bioenergetics in Hyperglycemic Rats

Cardiac glycosides are natural compounds used for the treatment of cardiovascular disorders. Although originally prescribed for cardiovascular diseases, more recently, they have been rediscovered for their potential use in the treatment of cancer. Proscillaridin A (PSD-A), a cardiac glycoside component of Urginea maritima, has been reported to exhibit anticancer activity. However, the cellular targets and anticancer mechanism of PSD-A in various cancers including lung cancer remain largely unexplored. In the present study, we found that PSD-A inhibits growth and induces apoptosis in A549 lung adenocarcinoma cells. The anticancer activity of PSD-A was found to be associated with the activation of JNK, induction of ER stress, mitochondrial dysfunction, and inhibition of STAT3 activation. PSD-A induces oxidative stress as evidenced from ROS generation, GSH depletion, and decreased activity of TrxR1. PSD-A-mediated ER stress was verified by increased phosphorylation of eIF2&#x03B1; and expression of its downstream effector proteins ATF4, CHOP, and caspases-4. PSD-A triggered apoptosis by inducing JNK (1/2) activation, increasing bax/bcl-2 ratio, dissipating mitochondrial membrane potential, and inducing cleavage of caspases and PARP. Further study revealed that PSD-A inhibits both constitutive and inducible STAT3 activations and decreases STAT3 DNA-binding activity. Moreover, PSD-A-mediated inhibition of STAT3 activation was found to be associated with increased SHP-1 expression, decreased phosphorylation of Src, and binding of PSD-A with STAT3 SH2 domain. Finally, STAT3 knockdown by shRNA inhibited growth and enhanced apoptotic efficacy of PSD-A. Taken together, the data suggest that PSD-A could be developed into a potential therapeutic agent against lung adenocarcinoma.

Amara Maryam

Tahir Mehmood

Qiulong Yan

Yongming Li

Muhammad Khan

Tonghui Ma

Proscillaridin A Promotes Oxidative Stress and ER Stress, Inhibits STAT3 Activation, and Induces Apoptosis in A549 Lung Adenocarcinoma Cells

Bing-rong Zhou

Li-wen Ma

Juan Liu

Jia-an Zhang

Yang Xu

Di Wu

Felicia Permatasari

Dan Luo

Corrigendum to &#x201C;Protective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin&#x201D;

Zhenquan Jia

Pon Velayutham Anandh Babu

Wei Chen

Xiaolun Sun

Natural Products Targeting on Oxidative Stress and Inflammation: Mechanisms, Therapies, and Safety Assessment

Oxidative stress is an important inducement in ovarian aging which results in fecundity decline in human and diverse animals. As a potent antioxidant, grape seed proanthocyanidin extract (GSPE) was investigated to ameliorate chicken ovarian aging in this study. Firstly, ovarian antioxidant capacity of hens at different ages (90, 150, 280, and 580 days old) was compared to elucidate its age-related changes. Subsequently, a D-gal-induced (2.5&#x2009;mg/mL) aging ovarian model was established and the cultured ovarian tissues were treated with GSPE at 5&#x2009;&#x03BC;g/mL for 72&#x2009;h to evaluate the putative attenuating effects of GSPE on ovarian aging. Meanwhile, ovaries of D280 (young) and D580 (old) were treated with GSPE for 72&#x2009;h in culture to verify the protective effects of GSPE on natural aging ovary. The results showed that GSPE could rescue the antioxidant capacity decline by increasing the antioxidase activities and their gene expression in either D-gal-induced or natural aging ovaries. Moreover, GSPE could maintain the homeostasis between cell proliferation and apoptosis in the D-gal-induced and natural aging ovaries, as well as alleviate D-gal-induced nucleus chromatin condensation in the ovarian granulosa cells. In conclusion, GSPE treatment can effectively prevent the ovarian aging process in hens by reducing oxidative stress.

Xingting Liu

Xin Lin

Yuling Mi

Jian Li

Caiqiao Zhang

Grape Seed Proanthocyanidin Extract Prevents Ovarian Aging by Inhibiting Oxidative Stress in the Hens

About this journal

Oxidative Medicine and Cellular Longevity publishes research involving cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, and metabolism.

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Chief Editor&nbsp;Dr Vasquez-Vivar has experience in free radical and redox biology research including the discovery of the role of tetrahydrobiopterin in the regulation of superoxide generation by endothelial and neuronal nitric oxide synthase.

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Oxidative Medicine and Cellular Longevity - Table of contents 2018

Oxidative Medicine and Cellular Longevity | Hindawi

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Oxidative Medicine and Cellular Longevity publishes research involving cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, and metabolism.

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Oxidative Medicine and Cellular Longevity

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