Protective effects of vitamin E on aluminium sulphate-induced testicular damage

2020 ◽  
Vol 36 (4) ◽  
pp. 215-227 ◽  
Author(s):  
Ozal Ulfanov ◽  
Nazli Cil ◽  
Esat Adiguzel
Keyword(s):  
Vitamin E ◽  
Male Infertility ◽  
Germinal Epithelium ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Protective Effects ◽  
Testicular Damage ◽  
Cell Series ◽  
Control Sham

Male infertility can be caused by environmental factors, genetic defects, physiological and endocrine deficiencies and testicular pathologies. Aluminium (Al) can cause male infertility through a number of mechanisms. The aim of our study was thus to determine whether vitamin E (VitE) has protective effects on Al-induced testicular damage, which was determined according to sperm counts and morphology and using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method. Thirty-four male Wistar rats (250–300 g) were randomly assigned to control (no procedures performed; n = 6) or 0.2 mL intraperitoneal injection group ( n = 7 each; three times per week for 4 weeks): sham (distilled water), 10 mg/kg Al, 500 mg/kg VitE and 10 mg/kg Al plus 500 mg/kg VitE (Al + VitE). Sperm samples were evaluated for andrological parameters. The testes were examined by haematoxylin/eosin. The epithelial thickness and areas were calculated and Johnsen scores were determined for the germinal epithelium; the apoptotic indices were determined from TUNEL staining. For Al, the bonds between the germinal epithelial cells were broken in some tubules, and there were unidentified cells in the lumen of some tubules. For control, sham and VitE, normal morphology of the germinal epithelium was generally preserved. With Al + VitE, the full germinal epithelium cell series was maintained, with only mature sperm in the lumen. TUNEL-positive cells were significantly higher with Al compared to control and sham ( p < 0.05). For Al + VitE, the number of apoptotic cells was reduced compared to Al alone and was therefore similar to control, sham and VitE ( p > 0.05). Our findings show that Al caused testicular damage. VitE reduced the number of apoptotic cells during the damage caused by Al.

Ischemic preconditioning and morphine attenuate myocardial apoptosis and infarction after ischemia-reperfusion in rabbits: role of δ-opioid receptor

2004 ◽  
Vol 287 (4) ◽  
pp. H1786-H1791 ◽  
Author(s):  
Shinji Okubo ◽  
Yujirou Tanabe ◽  
Kenji Takeda ◽  
Michihiko Kitayama ◽  
Seiyu Kanemitsu ◽  
...  
Keyword(s):  
Infarct Size ◽  
Opioid Receptor ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Apoptotic Cells ◽  
Protective Effects ◽  
Δ Opioid Receptor

We examined whether ischemic preconditioning (IPC) attenuates ischemia-reperfusion injury, in part, by decreasing apoptosis and whether the δ-opioid receptor (DOR) plays a pivotal role in the regulation of apoptosis. Rabbits were subjected to 30-min coronary artery occlusion (CAO) and 180 min of reperfusion. IPC was elicited with four cycles of 5-min ischemia and 10-min reperfusion before CAO. Morphine (0.3 mg/kg iv) was given 15 min before CAO. Naloxone (Nal; 10 mg/kg iv) and naltrindole (Nti; 10 mg/kg iv), the respective nonselective and selective DOR antagonists were given 10 min before either morphine or IPC. Infarct size (%risk area) was reduced from 46 ± 3.8 in control to 11.6 ± 1.0 in IPC and 19.5 ± 3.8 in the morphine group (means ± SE; P < 0.001 vs. control). Nal blocked the protective effects of IPC and morphine, as shown by the increase in infarct size to 38.6 ± 7.2 and 44.5 ± 1.8, respectively. Similarly, Nti blocked IPC and morphine-induced protection. The percentage of apoptotic cells (revealed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay) decreased in IPC (3.6 ± 1.9) and morphine groups (5.2 ± 1.2) compared with control group (12.4 ± 1.6; P < 0.001). Nti pretreatment increased apoptotic cells 11.2 ± 2.2% in IPC and 12.1 ± 0.8% in morphine groups. Nal failed to block inhibition of apoptosis in the IPC group (% of cells: 5.7 ± 1.3 vs. 3.6 ± 1.9 in IPC alone; P > 0.05). These results were also confirmed by nucleosomal DNA laddering pattern. We conclude that IPC reduces lethal injury, in part, by decreasing apoptosis after ischemia-reperfusion and activation of the DOR may play a crucial role in IPC or morphine-induced myocardial protection.

scholarly journals Protective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Bing-rong Zhou ◽  
Li-wen Ma ◽  
Juan Liu ◽  
Jia-an Zhang ◽  
Yang Xu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Human Skin ◽  
Ex Vivo ◽  
P53 Protein ◽  
Ultraviolet B ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Apoptotic Cells ◽  
Protective Effects ◽  
Bax Protein

Aim. We explored the effects of soy oligopeptides (SOP) in ultraviolet B- (UVB-) induced acute photodamage of human skin in vivo and foreskin ex vivo. Methods. We irradiated the forearm with 1.5 minimal erythemal dose (MED) of UVB for 3 consecutive days, establishing acute photodamage of skin, and topically applied SOP. Erythema index (EI), melanin index, stratum corneum hydration, and transepidermal water loss were measured by using Multiprobe Adapter 9 device. We irradiated foreskin ex vivo with the same dose of UVB (180 mJ/cm2) for 3 consecutive days and topically applied SOP. Sunburn cells were detected by using hematoxylin and eosin staining. Apoptotic cells were detected by using terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Cyclobutane pyrimidine dimers (CPDs), p53 protein, Bax protein, and Bcl-2 protein were detected by using immunohistochemical staining. Results. Compared with UVB group, UVB-irradiated skin with topically applied SOP showed significantly decreased EI. Compared with UVB group, topical SOP significantly increased Bcl-2 protein expression and decreased CPDs-positive cells, sunburn cells, apoptotic cells, p53 protein expression, and Bax protein expressions in the epidermis of UVB-irradiated foreskin. Conclusion. Our study demonstrated that topical SOP can protect human skin against UVB-induced photodamage.

scholarly journals Host-cell apoptosis inTaenia solium-induced brain granulomas in naturally infected pigs

Parasitology ◽  
2008 ◽  
Vol 135 (10) ◽  
pp. 1237-1242 ◽  
Author(s):  
C. S. SIKASUNGE ◽  
I. K. PHIRI ◽  
M. V. JOHANSEN ◽  
A. L. WILLINGHAM ◽  
P. S. LEIFSSON
Keyword(s):  
T Lymphocytes ◽  
Normal Cell ◽  
Taenia Solium ◽  
Cell Types ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Host Cell Apoptosis ◽  
Cellular Immune

SUMMARYTo assess whether apoptosis occurs in pig brain granulomas due toTaenia soliumcysticerci, brain tissues from 30 pigs naturally infected withT. soliumcysticercosis were evaluated by terminal deoxynucleotidyl transferase-end labelling (TUNEL) staining. In addition, tissues were stained with CD3 marker to identify T lymphocytes. Examination of TUNEL-stained tissues showed apoptotic cells in early lesions that contained viable cysticerci. Apoptotic cells were primarily found interspersed with normal cell types, and were mostly located in the inflammatory infiltrate. Late or advanced granulomas with disintegrated scolices did not show TUNEL-positive cells. CD3+ cells were found in both early and advanced lesions and apoptosis mainly co-localized with CD3+ T lymphocytes. This suggests that these cells are constantly undergoing apoptosis and thus die as soon as they arrive at the site of infection. Apoptosis indeed may be one way by whichT. soliumcysticerci down-regulate the host's cellular immune response in early cysticercosis. Therefore, further research is needed to establish if other cells besides T-lymphocytes are also a target for destruction by cysticerci in early cysticercosis as well as studies to assess if cysteine protease is expressed by viable cysticerciin situ.

scholarly journals Cardiac Protective Effect of Kirenol against Doxorubicin-Induced Cardiac Hypertrophy in H9c2 Cells through Nrf2 Signaling via PI3K/AKT Pathways

2021 ◽  
Vol 22 (6) ◽  
pp. 3269
Author(s):  
Abdullah M. Alzahrani ◽  
Peramaiyan Rajendran ◽  
Vishnu Priya Veeraraghavan ◽  
Hamza Hanieh
Keyword(s):  
Oxidative Stress ◽  
Biologically Active ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Cardiac Damage ◽  
Stress Markers ◽  
Nrf2 Signaling Pathway ◽  
Study Results

Kirenol (KRL) is a biologically active substance extracted from Herba Siegesbeckiae. This natural type of diterpenoid has been widely adopted for its important anti-inflammatory and anti-rheumatic properties. Despite several studies claiming the benefits of KRL, its cardiac effects have not yet been clarified. Cardiotoxicity remains a key concern associated with the long-term administration of doxorubicin (DOX). The generation of reactive oxygen species (ROS) causes oxidative stress, significantly contributing to DOX-induced cardiac damage. The purpose of the current study is to investigate the cardio-protective effects of KRL against apoptosis in H9c2 cells induced by DOX. The analysis of cellular apoptosis was performed using the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining assay and measuring the modulation in the expression levels of proteins involved in apoptosis and Nrf2 signaling, the oxidative stress markers. Furthermore, Western blotting was used to determine cell survival. KRL treatment, with Nrf2 upregulation and activation, accompanied by activation of PI3K/AKT, could prevent the administration of DOX to induce cardiac oxidative stress, remodeling, and other effects. Additionally, the diterpenoid enhanced the activation of Bcl2 and Bcl-xL, while suppressing apoptosis marker proteins. As a result, KRL is considered a potential agent against hypertrophy resulting from cardiac deterioration. The study results show that KRL not only activates the IGF-IR-dependent p-PI3K/p-AKT and Nrf2 signaling pathway, but also suppresses caspase-dependent apoptosis.

scholarly journals The anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on acrylamide-induced neurotoxicity in rats

2020 ◽  
Author(s):  
Jie Guo ◽  
Xiaolu Cao ◽  
Xianmin Hu ◽  
Shulan Li ◽  
Jun Wang
Keyword(s):  
Oxidative Stress ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background: Acrylamide (ACR) formed during heating of tobacco and carbohydrate-rich food as well as widely applied in industries has been known as a well-established neurotoxic pollutant. Although the precise mechanism is unclear, enhanced apoptosis, oxidative stress and inflammation have been demonstrated to contribute to the ACR-induced neurotoxicity. In this study, we assessed the possible anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin, the most active component in a popular spice known as turmeric, on the neurotoxicity caused by ACR in rats.Methods: Curcumin at the dose of 50 and 100 mg/kg was orally given to ACR- intoxicated Sprague-Dawley rats exposed by ACR at 40mg/kg for 4 weeks. All rats were subjected to behavioral analysis. The HE staining and terminal deoxynucleotidyl transferase mediated dUTP nick end labelling (TUNEL) staining were used to detect histopathological changes and apoptotic cells, respectively. The mRNA and protein expressions of apoptosis-related molecule telomerase reverse transcriptase (TERT) were detected using real-time PCR and immunohistochemistry, respectively. The contents of malondialdehyde (MDA) and glutathione (GSH) as well as the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were measured as the indicators for evaluating the level of oxidative stress in brain. The levels of pro-inflammatory cytokinestumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the cerebral homogenates were detected using ELISA assay.Results: ACR-induced weigh loss, deficits in motor function as well as pathological alterations in brains were significantly improved in rats administrated with 50 and 100 mg/kg curcumin. TUNEL-positive apoptotic cells in curcumin-treated ACR intoxicated brains were less than those in the ACR model group. Curcumin administration especially at the dose of 100 mg/kg upregulated the TERT mRNA expression and enhanced the number of TERT-positive cells in ACR-intoxicated cortex tissues. Moreover, curcumin treatment reduced the concentrations of TNF-α, IL-1β and MDA, while increased the GSH contents as well as the SOD and GSH-Px activities in the cerebral homogenates, in comparison to ACR control group.Conclusions: These data suggested the anti-apoptotic, antioxidant and anti-inflammatory effects of curcumin on ACR-induced neurotoxicity in rats. Maintaining TERT-related anti-apoptotic function might be one mechanism underlying the protective effect of curcumin on ACR-intoxicated brains.

scholarly journals Therapeutic and protective effects of autologous serum in amikacin-induced ototoxicity

2017 ◽  
Vol 132 (1) ◽  
pp. 33-40 ◽  
Author(s):  
I B Arslan ◽  
G G Aslan ◽  
G C Mercan ◽  
S Vatansever ◽  
I Cukurova ◽  
...  
Keyword(s):  
Otoacoustic Emissions ◽  
Spiral Ganglion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Autologous Serum ◽  
Control Group ◽  
Apoptotic Cells ◽  
Protective Effects ◽  
Spiral Limbus ◽  
Group A ◽  
Group B

AbstractObjective:Possible therapeutic and protective benefits of intratympanic autologous serum application in amikacin-induced ototoxicity were investigated.Methods:Twenty-four guinea pigs were separated equally into two groups: therapeutic (group A) and protective (group B). Transient evoked otoacoustic emissions were recorded before and after autologous serum application. Apoptotic cells were identified in the organ of Corti, spiral limbus and spiral ganglion by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (‘TUNEL’) method.Results:Transient evoked otoacoustic emission responses at 1, 1.4 and 2.8 kHz improved without significance after autologous serum application in group A (p> 0.05). A significantly protective effect of autologous serum was determined at 4 kHz in group B (p< 0.05). There were significantly fewer apoptotic cells at the spiral limbus in the therapeutic and protective groups compared to the control group (p< 0.05).Conclusion:Autologous serum may offer protection against ototoxicity-induced hearing loss, but it cannot restore hearing. Immunohistochemically, autologous serum significantly decreases activation of the intrinsic pathway of pro-apoptotic signalling in mesenchymal cells compared to neurons and neurosensory cells.

scholarly journals Sphingosine 1-Phosphate Affects Cytokine-Induced Apoptosis in Rat Pancreatic Islet β-Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (10) ◽  
pp. 4705-4712 ◽  
Author(s):  
Suzanne G. Laychock ◽  
Shawn M. Sessanna ◽  
Mei-Hui Lin ◽  
Lucy D. Mastrandrea
Keyword(s):  
Pancreatic Islet ◽  
Cell Apoptosis ◽  
Islet Cells ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Cell Protein ◽  
Tunel Staining ◽  
Protective Effects ◽  
Β Cells ◽  
Sphingosine 1 Phosphate ◽  
Induced Apoptosis

Cytokines mediate pancreatic islet β-cell apoptosis and necrosis, leading to loss of insulin secretory capacity and type 1 diabetes mellitus. The cytokines, IL-1β and interferon-γ, induced terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) staining of rat islet cells within 48 h by about 25–30%, indicative of apoptosis and/or necrosis. Sphingosine 1-phosphate (S1P) at nanomolar concentrations significantly reduced islet cell cytokine-induced TUNEL staining. Similar effects were observed in INS-1 cells. The dihydro analog of S1P also reduced the percentage of TUNEL stained islet and INS-1 cells, whereas the S1P receptor antagonist BML-241 blocked the protective effects. Pertussis toxin did not affect the S1P protective response. In the presence of a phospholipase C antagonist, U73122, there was significant inhibition of the S1P protective effects against apoptosis/necrosis. S1P stimulated INS-1 cell protein kinase C activity. Carbamylcholine chloride acting through muscarinic receptors also inhibited cytokine-induced TUNEL staining in pancreatic islet cells. S1P and/or dihydro-S1P also antagonized cytokine-induced increases in cytochrome c release from mitochondria and caspase-3 activity in INS-1 cells, which are indicative of cell apoptosis vs. necrosis. S1P failed to affect nitric oxide synthase activity after 48 h. Thus, the evidence suggests that S1P acting on S1P receptors coupled to Gq mediates protective effects on islet β-cells against cytokine-induced apoptosis.

scholarly journals Caffeic Acid Phenethyl Ester with Mesenchymal Stem Cells Improve Behavioral and Histopathological Changes in the Rat Model of Parkinson' Disease

2021 ◽  
Author(s):  
Khojasteh Rahimi Jaberi ◽  
◽  
Manouchehr Safari ◽  
Vahid Semnani ◽  
Hamid Reza Sameni ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Caffeic Acid ◽  
Dopaminergic Neurons ◽  
Intranasal Administration ◽  
Caffeic Acid Phenethyl Ester ◽  
Substantia Nigra Pars Compacta ◽  
Tunel Staining ◽  
Apoptotic Cells ◽  
Protective Effects

Introduction: Parkinson's disease (PD) is the result of the destruction of Dopaminergic neurons in the brain. The aim of this study was to investigate the protective effects of natural antioxidants such as caffeic acid phenethyl ester for the maintenance of these neurons. Methods: Caffeic acid phenethyl ester (CAPE) is one of the main ingredients of Propolis. Intranasal administration of (1-methyl-4-phenyl-2;3;4;6-tetrahydropyridine) MPTP was used to generate PD model in rats. 2× 106 bone marrow stem cells (BMSCs) were injected from tail vein. Behavioral test, Immunohistochemistry, DiI, cresyl fast violet, TUNEL staining were evaluated, 2 weeks after treatment. Results: DiI staining method revealed in all treatment groups using stem cells, the cells migrated to the substantia nigra pars compacta after injection. Treatment with CAPE significantly protects dopaminergic neurons from MPTP. The highest number of tyrosine hydroxylase (TH (positive neurons was seen in group Pre CAPE+PD+Stem cell. The number of TH+ cells in all groups that received CAPE was significant in compared to groups that received the stem cells only (P <0.001). Intranasal administration of MPTP significantly increase the number of apoptotic cells. The lowest number of apoptotic cells was in group Pre CAPE+PD+ Stem cell. Conclusion: The results showed that the use of CAPE and stem cells in Parkinson's rats caused a significant reduction in the apoptotic cells.

The Protective Effect of Metformin against Oxandrolone-Induced Infertility in Male Rats

2020 ◽  
Vol 26 ◽  
Author(s):  
Abdulqader Fadhil Abed ◽  
Yazun Bashir Jarrar ◽  
Hamzeh J Al-Ameer ◽  
Wajdy Al-Awaida ◽  
Su-Jun Lee
Keyword(s):  
Gene Expression ◽  
Male Infertility ◽  
Protective Effect ◽  
Histological Examination ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Male Rats ◽  
P Value ◽  
Protective Effects ◽  
Rt Pcr

Background: Oxandrolone is a synthetic testosterone analogue that is widely used among bodybuilders and athletes. However, oxandrolone causes male infertility. Recently, it was found that metformin reduces the risk of infertility associated with diabetes mellitus. Aim: This study aimed to investigate the protective effects of metformin against oxandrolone-induced infertility in male rats. Methods: Rats continuously received one of four treatments (n=7) over 14 days: control DMSO administration, oxandrolone administration, metformin administration, or co-administration of oxandrolone and metformin. Doses were equivalent to those used for human treatment. Subsequently, testicular and blood samples were collected for morphological, biochemical, and histological examination. In addition, gene expression of the testosterone synthesizing enzyme CYP11A1 was analyzed in the testes using RT-PCR. Results: Oxandrolone administration induced male infertility by significantly reducing relative weights of testes by 48%, sperm count by 82%, and serum testosterone levels by 96% (ANOVA, P value < 0.05). In addition, histological examination determined that oxandrolone caused spermatogenic arrest which was associated with 2-fold downregulation of testicular CYP11A1 gene expression. However, co-administration of metformin with oxandrolone significantly ameliorated toxicological alterations induced by oxandrolone exposure (ANOVA, P value < 0.05). Conclusion: Metformin administration protected against oxandrolone-induced infertility in male rats. Further clinical studies are needed to confirm the protective effect of metformin against oxandrolone-induced infertility among athletes.

scholarly journals Selenium deficiency induces spleen pathological changes in pigs by decreasing selenoprotein expression, evoking oxidative stress, and activating inflammation and apoptosis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Shuang Li ◽  
Wenjuan Sun ◽  
Kai Zhang ◽  
Jiawei Zhu ◽  
Xueting Jia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
The Body ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Antioxidant Systems ◽  
Tunel Staining ◽  
White Pulp ◽  
Sibling Pairs ◽  
Se Deficiency ◽  
Spleen Index

Abstract Background The immune system is one aspect of health that is affected by dietary selenium (Se) levels and selenoprotein expression. Spleen is an important immune organ of the body, which is directly involved in cellular immunity. However, there are limited reports on Se levels and spleen health. Therefore, this study established a Se-deficient pig model to investigate the mechanism of Se deficiency-induced splenic pathogenesis. Methods Twenty-four pure line castrated male Yorkshire pigs (45 days old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into two equal groups and fed Se-deficient diet (0.007 mg Se/kg) or Se-adequate diet (0.3 mg Se/kg) for 16 weeks. At the end of the trial, blood and spleen were collected to assay for erythroid parameters, the osmotic fragility of erythrocytes, the spleen index, histology, terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining, Se concentrations, the selenogenome, redox status, and signaling related inflammation and apoptosis. Results Dietary Se deficiency decreased the erythroid parameters and increased the number of osmotically fragile erythrocytes (P < 0.05). The spleen index did not change, but hematoxylin and eosin and TUNEL staining indicated that the white pulp decreased, the red pulp increased, and splenocyte apoptosis occurred in the Se deficient group. Se deficiency decreased the Se concentration and selenoprotein expression in the spleen (P < 0.05), blocked the glutathione and thioredoxin antioxidant systems, and led to redox imbalance. Se deficiency activated the NF-κB and HIF-1α transcription factors, thus increasing pro-inflammatory cytokines (IL-1β, IL-6, IL-8, IL-17, and TNF-α), decreasing anti-inflammatory cytokines (IL-10, IL-13, and TGF-β) and increasing expression of the downstream genes COX-2 and iNOS (P < 0.05), which in turn induced inflammation. In addition, Se-deficiency induced apoptosis through the mitochondrial pathway, upregulated apoptotic genes (Caspase3, Caspase8, and Bak), and downregulated antiapoptotic genes (Bcl-2) (P < 0.05) at the mRNA level, thus verifying the results of TUNEL staining. Conclusions These results indicated that Se deficiency induces spleen injury through the regulation of selenoproteins, oxidative stress, inflammation and apoptosis.

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