Developmental Neurotoxicity of Arsenic: Involvement of Oxidative Stress and Mitochondrial Functions

We tested the effects of swimming training and insulin therapy, either alone or in combination, on the intracellular calcium ([Ca2+]i) homeostasis, oxidative stress, and mitochondrial functions in diabetic rat hearts. Male Wistar rats were separated into control, diabetic, or diabetic plus insulin groups. Type 1 diabetes mellitus was induced by streptozotocin (STZ). Insulin-treated groups received 1 to 4 UI of insulin daily for 8 wk. Each group was divided into sedentary or exercised rats. Trained groups were submitted to swimming (90 min/day, 5 days/wk, 8 wk). [Ca2+]i transient in left ventricular myocytes (LVM), oxidative stress in LV tissue, and mitochondrial functions in the heart were assessed. Diabetes reduced the amplitude and prolonged the times to peak and to half decay of the [Ca2+]i transient in LVM, increased NADPH oxidase-4 (Nox-4) expression, decreased superoxide dismutase (SOD), and increased carbonyl protein contents in LV tissue. In isolated mitochondria, diabetes increased Ca2+ uptake, susceptibility to permeability transition pore (MPTP) opening, uncoupling protein-2 (UCP-2) expression, and oxygen consumption but reduced H2O2 release. Swimming training corrected the time course of the [Ca2+]i transient, UCP-2 expression, and mitochondrial Ca2+ uptake. Insulin replacement further normalized [Ca2+]i transient amplitude, Nox-4 expression, and carbonyl content. Alongside these benefits, the combination of both therapies restored the LV tissue SOD and mitochondrial O2 consumption, H2O2 release, and MPTP opening. In conclusion, the combination of swimming training with insulin replacement was more effective in attenuating intracellular Ca2+ disruptions, oxidative stress, and mitochondrial dysfunctions in STZ-induced diabetic rat hearts.

Download Full-text

Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Antioxidants ◽

10.3390/antiox10020229 ◽

2021 ◽

Vol 10 (2) ◽

pp. 229

Author(s):

JunHyuk Woo ◽

Hyesun Cho ◽

YunHee Seol ◽

Soon Ho Kim ◽

Chanhyeok Park ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Computational Models ◽

Neuronal Damage ◽

Living Organism ◽

The Body ◽

Mitochondrial Functions ◽

A Cell ◽

The Brain ◽

And Oxidative Stress

The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5′-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.

Download Full-text

Effects of Different Music on HEK293T Cell Growth and Mitochondrial Functions

EXPLORE ◽

10.1016/j.explore.2022.01.002 ◽

2022 ◽

Author(s):

Qian Feng ◽

Lin Wang ◽

Yu Chen ◽

Mengmei Li ◽

Jie Teng ◽

...

Keyword(s):

Cell Growth ◽

Hek293t Cell ◽

Mitochondrial Functions ◽

And Mitochondrial Functions

Download Full-text

Cytoprotective Effects of N-Acetylcysteine on Streptozotocin- Induced Oxidative Stress and Apoptosis in RIN-5F Pancreatic β-Cells

Cellular Physiology and Biochemistry ◽

10.1159/000495200 ◽

2018 ◽

Vol 51 (1) ◽

pp. 201-216 ◽

Cited By ~ 8

Author(s):

Arwa M.T. Al-Nahdi ◽

Annie John ◽

Haider Raza

Keyword(s):

Oxidative Stress ◽

Insulin Secretion ◽

Molecular Mechanisms ◽

Protective Action ◽

Mitochondrial Enzymes ◽

Partial Recovery ◽

Β Cells ◽

Pancreatic Β Cells ◽

Mitochondrial Energy Metabolism ◽

Mitochondrial Functions

Background/Aims: Numerous studies have reported overproduction of reactive oxygen species (ROS) and alterations in mitochondrial energy metabolism in the development of diabetes and its complications. The potential protective effects of N-acetylcysteine (NAC) in diabetes have been reported in many therapeutic studies. NAC has been shown to reduce oxidative stress and enhance redox potential in tissues protecting them against oxidative stress associated complications in diabetes. In the current study, we aimed to investigate the molecular mechanisms of the protective action of NAC on STZ-induced toxicity in insulin secreting Rin-5F pancreatic β-cells. Methods: Rin-5F cells were grown to 80% confluence and then treated with 10mM STZ for 24h in the presence or absence of 10mM NAC. After sub-cellular fractionation, oxidative stress, GSH-dependent metabolism and mitochondrial respiratory functions were studied using spectrophotometric, flow cytometric and Western blotting techniques. Results: Our results showed that STZ-induced oxidative stress and apoptosis caused inhibition in insulin secretion while NAC treatment restored the redox homeostasis, enhanced insulin secretion in control cells and prevented apoptosis in STZ-treated cells. Moreover, NAC attenuated the inhibition of mitochondrial functions induced by STZ through partial recovery of the mitochondrial enzymes and restoration of membrane potential. STZ-induced DNA damage and expression of apoptotic proteins were significantly inhibited in NAC-treated cells. Conclusion: Our results suggest that the cytoprotective action of NAC is mediated via suppression of oxidative stress and apoptosis and restoration of GSH homeostasis and mitochondrial bioenergetics. This study may, thus, help in better understanding the cellular defense mechanisms of pancreatic β-cells against STZ-induced cytotoxicity.

Download Full-text

Mitotype Interacts With Diet to Influence Longevity, Fitness, and Mitochondrial Functions in Adult Female Drosophila

Frontiers in Genetics ◽

10.3389/fgene.2018.00593 ◽

2018 ◽

Vol 9 ◽

Cited By ~ 4

Author(s):

Samuel G. Towarnicki ◽

J. William O. Ballard

Keyword(s):

Adult Female ◽

Mitochondrial Functions ◽

And Mitochondrial Functions

Download Full-text

Effects of dietary tributyrin on intestinal mucosa development, mitochondrial function and AMPK-mTOR pathway in weaned pigs

Journal of Animal Science and Biotechnology ◽

10.1186/s40104-019-0394-x ◽

2019 ◽

Vol 10 (1) ◽

Author(s):

Chunchun Wang ◽

Shuting Cao ◽

Zhuojun Shen ◽

Qihua Hong ◽

Jie Feng ◽

...

Keyword(s):

Oxidative Stress ◽

Intestinal Mucosa ◽

Mitochondrial Function ◽

Control Group ◽

Mrna Levels ◽

Villus Height ◽

Weaned Pigs ◽

Glucose Transporter 2 ◽

Phosphorylation Level ◽

Mitochondrial Functions

Abstract Background The objective of this experiment was to investigate the influence of dietary tributyrin on intestinal mucosa development, oxidative stress, mitochondrial function and AMPK-mTOR signaling pathway. Methods Seventy-two pigs were divided into two treatments and received either a basal diet or the same diet supplemented with 750 mg/kg tributyrin. Each treatment has six replicates of six pigs. After 14 days, 6 pigs from each treatment were selected and the jejunal samples were collected. Results Results showed that supplemental tributyrin increased (P < 0.05) villus height and villus height: crypt depth of weaned pigs. Pigs fed tributyrin had greater (P < 0.05) RNA/DNA and protein/DNA ratios than pigs on the control group. The mRNA levels of sodium glucose transport protein-1 and glucose transporter-2 in the jejunum were upregulated (P < 0.05) in pigs fed the tributyrin diet. Dietary tributyrin supplementation lowered (P < 0.05) the malondialdehyde and hydrogen peroxide (H2O2) content in jejunum, enhanced (P < 0.05) the mitochondrial function, as demonstrated by decreased (P < 0.05) reactive oxygen species level and increased (P < 0.05) mitochondrial membrane potential. Furthermore, tributyrin increased (P < 0.05) mitochondrial DNA content and the mRNA abundance of genes related to mitochondrial functions, including peroxisomal proliferator-activated receptor-γ coactivator-1α, mitochondrial transcription factor A, nuclear respiratory factor-1 in the jejunum. Supplementation with tributyrin elevated (P < 0.05) the phosphorylation level of AMPK and inhibited (P < 0.05) the phosphorylation level of mTOR in jejunum compared with the control group. Conclusions These findings suggest that dietary supplementation with tributyrin promotes intestinal mucosa growth, extenuates oxidative stress, improves mitochondrial function and modulates the AMPK-mTOR signal pathway of weaned pigs.

Download Full-text

57 Carnosine prevents oxidative damage in myoblast cells derived from porcine skeletal muscle

Journal of Animal Science ◽

10.1093/jas/skz258.122 ◽

2019 ◽

Vol 97 (Supplement_3) ◽

pp. 59-59

Author(s):

Marie-France Palin ◽

Jérôme Lapointe ◽

Claude Gariépy ◽

Danièle Beaudry ◽

Claudia Kalbe

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Metal Ion ◽

Antioxidant Activities ◽

Radical Scavenging ◽

Biochemical Properties ◽

Antioxidant Enzyme Activities ◽

Antioxidant Genes ◽

Mitochondrial Functions ◽

Myoblast Cells

Abstract Carnosine (β-alanyl-L-histidine) is a molecule naturally and exclusively present in muscle food with the highest concentrations found in skeletal muscles and brain of the animal. Among its numerous biochemical properties, carnosine has antioxidant activity which include metal ion chelation and free radical scavenging. We have recently reported that high muscle carnosine content in pig is associated with better meat quality. Moreover, supplementing pigs with β-alanine reduced oxidative damage to Longissimus muscle (LM) lipids and proteins. Among previously reported antioxidant activities, carnosine was found to limit the production of reactive oxygen species (ROS) and increase antioxidant enzyme activities. However, these studies were mainly conducted in rodents and cell lines and mechanisms in play remain to be characterized. To determine the effect of carnosine in preventing oxidative damage and characterize the mechanisms in play, we have undertaken experiments using the progeny (myoblasts) of satellite cells isolated from the LM of newborn piglets. Cells were treated with carnosine (0, 10, 25 and 50 mM) for 48 h and were then either collected immediately or treated with H2O2 (0.3 mM, 1 h) to induce an oxidative stress. Our results showed that carnosine prevents oxidative stress through the reduction of total intracellular ROS and by modulating the antioxidant system in myoblasts.Carnosine increased the mRNA abundance of NEF2L2, a transcription factor activated by oxidative stress, and several of its downstream regulated antioxidant genes. Western blot analyses further suggest that the protective effect of carnosine on H2O2-induced oxidative stress is mediated through the p38 MAPK intracellular pathway. Finally, the addition of carnosine to H2O2-treated myoblasts increased the basal cellular oxygen consumption rate (OCR), the ATP-linked OCR and proton leaks, thus suggesting an effect of carnosine on mitochondrial functions. Taken together, these findings demonstrate the important role of carnosine in preventing oxidative damage in porcine muscle cells.

Download Full-text

Honeybush Extracts (Cyclopia spp.) Rescue Mitochondrial Functions and Bioenergetics against Oxidative Injury

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/1948602 ◽

2020 ◽

Vol 2020 ◽

pp. 1-14

Author(s):

Anastasia Agapouda ◽

Veronika Butterweck ◽

Matthias Hamburger ◽

Dalene de Beer ◽

Elizabeth Joubert ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Hot Water ◽

Human Neuroblastoma ◽

Atp Production ◽

Physiological Conditions ◽

Age Related ◽

Mitochondrial Functions ◽

Scientific Attention

Mitochondrial dysfunction plays a major role not only in the pathogenesis of many oxidative stress or age-related diseases such as neurodegenerative as well as mental disorders but also in normal aging. There is evidence that oxidative stress and mitochondrial dysfunction are the most upstream and common events in the pathomechanisms of neurodegeneration. Cyclopia species are endemic South African plants and some have a long tradition of use as herbal tea, known as honeybush tea. Extracts of the tea are gaining more scientific attention due to their phenolic composition. In the present study, we tested not only the in vitro mitochondria-enhancing properties of honeybush extracts under physiological conditions but also their ameliorative properties under oxidative stress situations. Hot water and ethanolic extracts of C. subternata, C. genistoides, and C. longifolia were investigated. Pretreatment of human neuroblastoma SH-SY5Y cells with honeybush extracts, at a concentration range of 0.1-1 ng/ml, had a beneficial effect on bioenergetics as it increased ATP production, respiration, and mitochondrial membrane potential (MMP) after 24 hours under physiological conditions. The aqueous extracts of C. subternata and C. genistoides, in particular, showed a protective effect by rescuing the bioenergetic and mitochondrial deficits under oxidative stress conditions (400 μM H2O2 for 3 hours). These findings indicate that honeybush extracts could constitute candidates for the prevention of oxidative stress with an impact on aging processes and age-related neurodegenerative disorders potentially leading to the development of a condition-specific nutraceutical.

Download Full-text

Acerola polysaccharides ameliorate high-fat diet-induced non-alcoholic fatty liver disease through reduction of lipogenesis and improvement of mitochondrial functions in mice

Food & Function ◽

10.1039/c9fo01611b ◽

2020 ◽

Vol 11 (1) ◽

pp. 1037-1048 ◽

Cited By ~ 2

Author(s):

Yuanyuan Hu ◽

Fawen Yin ◽

Zhongyuan Liu ◽

Hongkai Xie ◽

Yunsheng Xu ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Disease ◽

Fatty Liver ◽

Mitochondrial Function ◽

High Fat Diet ◽

Fatty Liver Disease ◽

High Fat ◽

Alcoholic Fatty Liver ◽

Mitochondrial Functions ◽

Alcoholic Fatty Liver Disease

Acerola polysaccharides ameliorate HFD-induced NAFLD by inhibiting lipogenesis, reducing oxidative stress and inflammation, and promoting the mitochondrial function in C57BL/6 mice.

Download Full-text