scholarly journals Imbalance of Autophagy and Apoptosis Induced by Oxidative Stress May Be Involved in Thyroid Damage Caused by Sleep Deprivation in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yongmei Li ◽  
Wei Zhang ◽  
Mengqi Liu ◽  
Qiuping Zhang ◽  
Zijie Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Sleep Deprivation ◽  
Total Antioxidant Capacity ◽  
Morphological Changes ◽  
Thyroid Stimulating Hormone ◽  
Deprivation Group ◽  
Total Antioxidant ◽  
Related Proteins

Many studies have shown that sleep deprivation can affect a wide range of tissues and organs, and most of these effects are related to oxidative stress. Oxidative stress can cause functional and morphological changes in cells, which are closely related to autophagy and apoptosis. In this study, we examined changes in thyroid morphology and function, oxidative stress, autophagy, and apoptosis in rats after sleep deprivation. Thyroid hormones, thyroid-stimulating hormone, functional substances required for the synthesis of thyroid hormones, and thyroid morphological observations were used to evaluate the changes and impairment of thyroid function. Methane dicarboxylic aldehyde and total antioxidant capacity were measured to assess oxidative stress in the thyroid. To evaluate the balance of autophagy and apoptosis, the expression of autophagy- and apoptosis-related proteins was examined by western blotting, and apoptotic cells were labeled with TUNEL staining. The body weight of rats in the sleep deprivation group decreased, but the relative weight of the thyroid gland increased. Sleep deprivation led to morphological changes in the thyroid. The levels of thyroid hormones and thyroid-stimulating hormone increased after sleep deprivation. Total antioxidant capacity decreased, and methane dicarboxylic aldehyde levels increased in the thyroid in the sleep deprivation group. Analysis of autophagy- and apoptosis-related proteins indicated that the microtubule-associated protein 1 light chain 3 beta- (LC3B-) and LC3A-II/I ratio and Beclin 1 levels significantly decreased in the sleep deprivation group and P62 levels significantly increased. The number of apoptotic cells in the thyroid gland of sleep-deprived rats increased significantly. Taken together, these results indicate that sleep deprivation can lead to oxidative stress in the thyroid and ultimately cause thyroid damage, which may be related to the imbalance of autophagy and apoptosis.

scholarly journals Autophagy Triggered by Oxidative Stress Appears to Be Mediated by the AKT/mTOR Signaling Pathway in the Liver of Sleep-Deprived Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Yongmei Li ◽  
Yuan Zhang ◽  
Guang Ji ◽  
Yiwei Shen ◽  
Nan Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sleep Deprivation ◽  
Signaling Pathway ◽  
Mammalian Target Of Rapamycin ◽  
Hepatic Function ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Deprivation Group ◽  
Mda Content ◽  
Related Proteins

Sleep deprivation adversely affects the digestive system. Multiple studies have suggested sleep deprivation and oxidative stress are closely related. Autophagy can be triggered by oxidative stress as a self-defense strategy to promote survival. In this study, we investigated the effects of sleep deprivation on liver functions, oxidative stress, and concomitant hepatocyte autophagy, as well as the associated pathways. Enzymatic and nonenzymatic biochemical markers in the serum were used to assess hepatic function and damage. To evaluate the occurrence of autophagy, expression of autophagy-related proteins was tested and autophagosomes were labeled. Additionally, methane dicarboxylic aldehyde (MDA), antioxidant enzymes, and the protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway were analyzed using chemical methods and a Western blot. Serum alanine transaminase, aspartate aminotransferase, and alkaline phosphatase increased in sleep-deprived rats. Total protein and albumin abundance was also abnormal. Sleep deprivation induced histopathological changes in the liver. The superoxide dismutase level decreased significantly in the liver of sleep-deprived rats. In contrast, the MDA content increased in the sleep deprivation group. Moreover, the microtubule-associated protein 1 light chain 3 beta (LC3B) II/I ratio and Beclin I content increased considerably in the sleep-deprived rats, while p62 levels decreased. Sleep deprivation apparently inhibited the AKT/mTOR signaling pathway. We conclude that sleep deprivation can induce oxidative stress and ultimately cause liver injury. Autophagy triggered by oxidative stress appears to be mediated by the AKT/mTOR pathway and plays a role in relieving oxidative stress caused by sleep deprivation.

Evaluation of Salivary Antioxidants and Oxidative Stress Markers in Male Smokers

2019 ◽  
Vol 22 (7) ◽  
pp. 496-501
Author(s):  
Fatemeh Ahmadi-Motamayel ◽  
Parisa Falsafi ◽  
Hamidreza Abolsamadi ◽  
Mohammad T. Goodarzi ◽  
Jalal Poorolajal
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Free Radicals ◽  
Antioxidant Capacity ◽  
Cigarette Smoke ◽  
Total Antioxidant Capacity ◽  
The Body ◽  
Total Antioxidant ◽  
The Mean ◽  
And Oxidative Stress

Background: Cigarette smoke free radicals can cause cellular damage and different diseases. All the body fluids have antioxidants which protect against free radicals. Objective: The aim of this study was to evaluate salivary total antioxidant capacity and peroxidase, uric acid and malondialdehyde levels in smokers and a nonsmoking control group. Methods: Unstimulated saliva was collected from 510 males. A total of 259 subjects were current smokers and 251 were non-smokers. The levels of salivary total antioxidant capacity, uric acid, peroxidase and malondialdehyde were measured using standard procedures. Data were analyzed with t test and ANOVA. Results: The smokers were younger and dental hygiene index was higher than healthy nonsmoking controls. The mean total antioxidant capacity in smokers and nonsmokers was 0.13±0.07 and 0.21±011, respectively (P=0.001). Smokers had significantly lower peroxidase and uric acid levels than healthy controls. In addition, the mean malondialdehyde levels in the smokers and nonsmokers were 4.55 ±2.61 and 2.79 ±2.21, respectively (P=0.001). Conclusion: Cigarette smoke produces free radical and oxidative stress, causing many side effects. Salivary antioxidant levels decreased and malondialdehyde levels increased in smokers, indicating the high oxidative stress among smokers compared to nonsmokers. Cigarette smoke had deleterious effects on main salivary antioxidants levels.

scholarly journals Total Antioxidant Capacity in HBV Carriers, a Promising Biomarker for Evaluating Hepatic Fibrosis: A Pilot Study

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 77
Author(s):  
Jing-Hua Wang ◽  
Sung-Bae Lee ◽  
Dong-Soo Lee ◽  
Chang-Gue Son
Keyword(s):  
Oxidative Stress ◽  
Chronic Hepatitis ◽  
Liver Fibrosis ◽  
Hepatitis B ◽  
Antioxidant Capacity ◽  
Chronic Hepatitis B ◽  
Hepatic Fibrosis ◽  
Total Antioxidant Capacity ◽  
Hbv Dna ◽  
Total Antioxidant

Oxidative stress plays a pivotal role in the progression of chronic hepatitis B; however, it is unclear whether the status of blood oxidative stress and antioxidant components differs depending on the degree of hepatic fibrosis. To explore the relationship between oxidative stress/antioxidant capacity and the extent of hepatic fibrosis, fifty-four subjects with liver fibrosis (5.5 ≤ liver stiffness measurement (LSM) score ≤ 16.0 kPa) by chronic hepatitis B virus (HBV) were analyzed. From the analysis of eight kinds of serum oxidative stress/antioxidant profiles and liver fibrosis degrees, the level of total antioxidant capacity (TAC) reflected a negative correlation with the severity of hepatic fibrosis (Pearson correlation, r = −0.35, p = 0.01). Moreover, TAC showed higher sensitivity (73.91%) than the aspartate transaminase (AST) to platelet ratio index (APRI, 56.52%) in the receiver operating characteristic (ROC) curves. Interestingly, the TAC level finely reflected the fibrosis degree in inactive carriers (HBV DNA < 2000 IU/mL), while the APRI did in active carriers (HBV DNA > 2000 IU/mL). In conclusion, TAC is a promising biomarker for evaluating the progression of liver fibrosis in patients with HBV, and this finding may indicate the involvement of TAC-composing factors in the pathogenesis of hepatic fibrosis in chronic HBV carriers.

scholarly journals Total Antioxidant Capacity and Lipid Peroxidation Status in Cervical Cancer Patients Compared with Women Without Cervical Cancer in Bangladesh

2021 ◽  
Vol 19 (4) ◽  
Author(s):  
Taslima Nigar ◽  
Annekathryn Goodman ◽  
Shahana Pervin
Keyword(s):  
Oxidative Stress ◽  
Cervical Cancer ◽  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Antioxidant Capacity ◽  
Cancer Patients ◽  
Total Antioxidant Capacity ◽  
Stress Index ◽  
Oxidative Stress Index ◽  
Total Antioxidant

Abstract Purpose Over the past several decades, research has suggested reactive oxygen species act as cofactors for cervical cancer development. The aim of this study is to evaluate the antioxidant and lipid peroxidation status in cervical cancer patients in Bangladesh. Methods From December 2017 to 2018, a cross-sectional observational study was conducted on 50 cervical cancer patients and 50 controls. Plasma levels of lipid peroxidation and total antioxidant capacity were measured. The Student’s t test was used for statistical analysis. P values less than 0.05 were taken as a level of significance. Results There was a significant reduction in total antioxidant levels in patients with cervical cancer, 972.77 ± 244.22 SD µmol equivalent to ascorbic acid/L, compared to normal controls, 1720.13 ± 150.81 SD µmol equivalent to ascorbic acid/L (P < 0.001). Levels of lipid peroxidation were found to be significantly higher in cervical cancer, 7.49 ± 2.13 SD µmol/L, than in women without cervical cancer, 3.28 ± 0.58 SD µmol/L (P < 0.001). The cervical cancer patients had significantly higher levels of oxidative stress index (0.83 ± 0.31) in comparison to controls (0.19 ± 0.04) (P < 0.001). Conclusion There was an increased oxidative stress index due to imbalance between lipid peroxidation generation and total antioxidant capacity in cervical cancer patients. Further studies are needed to explore the role of oxidative stress as a cofactor for cervical carcinogenesis.

scholarly journals Effect of the French Oak Wood Extract Robuvit on Markers of Oxidative Stress and Activity of Antioxidant Enzymes in Healthy Volunteers: A Pilot Study

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Martina Horvathova ◽  
Zuzana Orszaghova ◽  
Lucia Laubertova ◽  
Magdalena Vavakova ◽  
Peter Sabaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Antioxidant Capacity ◽  
Healthy Volunteers ◽  
Total Antioxidant Capacity ◽  
Trolox Equivalent Antioxidant Capacity ◽  
Total Antioxidant ◽  
Trolox Equivalent ◽  
Markers Of Oxidative Stress

We examinedin vitroantioxidant capacity of polyphenolic extract obtained from the wood of oakQuercus robur(QR), Robuvit, using TEAC (Trolox equivalent antioxidant capacity) method and the effect of its intake on markers of oxidative stress, activity of antioxidant enzymes, and total antioxidant capacity in plasma of 20 healthy volunteers. Markers of oxidative damage to proteins, DNA, and lipids and activities of Cu/Zn-superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were determined in the erythrocytes. We have found anin vitroantioxidant capacity of Robuvit of 6.37 micromole Trolox equivalent/mg of Robuvit. One month intake of Robuvit in daily dose of 300 mg has significantly decreased the serum level of advanced oxidation protein products (AOPP) and lipid peroxides (LP). Significantly increased activities of SOD and CAT as well as total antioxidant capacity of plasma after one month intake of Robuvit have been shown. In conclusion, we have demonstrated for the first time that the intake of Robuvit is associated with decrease of markers of oxidative stress and increase of activity of antioxidant enzymes and total antioxidant capacity of plasmain vivo.

Iodide Metabolism and Effects

2020 ◽  
pp. 25-33
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Dietary Supplement ◽  
Thyroid Function ◽  
Thyroid Stimulating Hormone ◽  
Hormone Synthesis ◽  
Serum Tsh ◽  
Tsh Stimulation ◽  
Sensitive Marker

Iodine (I2) is essential in the synthesis of thyroid hormones T4 and T3 and functioning of the thyroid gland. Both T3 and T4 are metabolically active, but T3 is four times more potent than T4. Our body contains 20-30 mg of I2, which is mainly stored in the thyroid gland. Iodine is naturally present in some foods, added to others, and available as a dietary supplement. Serum thyroid stimulating hormone (TSH) level is a sensitive marker of thyroid function. Serum TSH is increased in hypothyroidism as in Hashimoto's thyroiditis. In addition to regulation of thyroid function, TSH promotes thyroid growth. If thyroid hormone synthesis is chronically impaired, TSH stimulation eventually may lead to the development of a goiter. This chapter explores the iodide metabolism and effects of Hashimoto's disease.

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