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Antioxidants (Basel, Switzerland) Jul 2023Altered levels of heavy metals and essential elements have been associated with oxidative stress (OS) and metabolic and hormonal changes in women with polycystic ovary... (Review)
Review
Altered levels of heavy metals and essential elements have been associated with oxidative stress (OS) and metabolic and hormonal changes in women with polycystic ovary syndrome (PCOS). We aimed to summarize the knowledge on the association of heavy metals and essential elements with OS in PCOS. An electronic literature search using PubMed for studies published between January 2008 and April 2023 was conducted. We evaluated heavy metals and essential elements in relation to OS in PCOS in 15 articles. PCOS women had increased antimonium (Sb), cadmium (Cd), lead (Pb), mercury (Hg), arsenic (As), tellurium (Te), thallium (Tl) and osmium (Os) blood levels and decreased zinc (Zn) blood levels; the results of copper (Cu) blood levels were conflicting. Some studies showed a significant correlation between heavy metals (Sb, Cd, Pb, Hg, As, Te and Tl) and essential elements (Se, Zn, Cr, Ca, Mg and Cu) and markers of OS and chronic inflammation. Heavy metals (Sb, Cd, Pb and Hg) and essential elements (Zn, Cr, Se, Ca, Mg and Cu) were associated with metabolic and hormonal characteristics in PCOS. There might be a possible benefit from supplementation therapy in reducing OS and endocrinological problems related to PCOS. Our review confirmed an association between heavy metals and essential elements with OS in PCOS women. This systematic review is registered in PROSPERO under number CRD42023418453.
PubMed: 37507937
DOI: 10.3390/antiox12071398 -
Cells Aug 2023There is an increasing interest in biomarkers of nitric oxide dysregulation and oxidative stress to guide management and identify new therapeutic targets in patients... (Meta-Analysis)
Meta-Analysis Review
There is an increasing interest in biomarkers of nitric oxide dysregulation and oxidative stress to guide management and identify new therapeutic targets in patients with chronic obstructive pulmonary disease (COPD). We conducted a systematic review and meta-analysis of the association between circulating metabolites within the arginine (arginine, citrulline, ornithine, asymmetric, ADMA, and symmetric, SDMA dimethylarginine), transsulfuration (methionine, homocysteine, and cysteine) and folic acid (folic acid, vitamin B, and vitamin B) metabolic pathways and COPD. We searched electronic databases from inception to 30 June 2023 and assessed the risk of bias and the certainty of evidence. In 21 eligible studies, compared to healthy controls, patients with stable COPD had significantly lower methionine (standardized mean difference, SMD = -0.50, 95% CI -0.95 to -0.05, = 0.029) and folic acid (SMD = -0.37, 95% CI -0.65 to -0.09, = 0.009), and higher homocysteine (SMD = 0.78, 95% CI 0.48 to 1.07, < 0.001) and cysteine concentrations (SMD = 0.34, 95% CI 0.02 to 0.66, = 0.038). Additionally, COPD was associated with significantly higher ADMA (SMD = 1.27, 95% CI 0.08 to 2.46, = 0.037), SDMA (SMD = 3.94, 95% CI 0.79 to 7.08, = 0.014), and ornithine concentrations (SMD = 0.67, 95% CI 0.13 to 1.22, = 0.015). In subgroup analysis, the SMD of homocysteine was significantly associated with the biological matrix assessed and the forced expiratory volume in the first second to forced vital capacity ratio, but not with age, study location, or analytical method used. Our study suggests that the presence of significant alterations in metabolites within the arginine, transsulfuration, and folic acid pathways can be useful for assessing nitric oxide dysregulation and oxidative stress and identifying novel treatment targets in COPD. (PROSPERO registration number: CRD42023448036.).
Topics: Humans; Cysteine; Nitric Oxide; Metabolomics; Arginine; Methionine; Racemethionine; Folic Acid; Homocysteine; Vitamins
PubMed: 37681911
DOI: 10.3390/cells12172180 -
Frontiers in Pharmacology 2023There is currently evidence suggesting that ursolic acid may exert a favorable influence on both anti-inflammatory and antioxidant impact. Nevertheless, the...
There is currently evidence suggesting that ursolic acid may exert a favorable influence on both anti-inflammatory and antioxidant impact. Nevertheless, the anti-inflammatory and antioxidant activities of ursolic acid have not been systematically evaluated. Consequently, this study aims to conduct a systematic review and meta-analysis regarding the impact of ursolic acid on markers of inflammatory and antioxidant activity in both animal models and systems. The search encompassed databases such as PubMed, Web of Science, Google Scholar, and ScienceDirect, up until May 2023. All eligible articles in English were included in the analysis. Standard mean difference (SMD) was pooled using a random-effects model, and the included studies underwent a thorough assessment for potential bias. The final review comprised 31 articles. In disease-model related studies, animal experiments have consistently shown that ursolic acid significantly reduced the levels of inflammatory parameters IL-1β, IL-6 and TNF-α in mouse tissues. In vitro studies have similarly showed that ursolic acid significantly reduced the levels of inflammatory parameters IL-1β, IL-6, IL-8 and TNF-α. Our results showed that ursolic acid could significantly elevate SOD and GSH levels, while significantly reducing MDA levels in animal tissues. The results of studies shown that ursolic acid significantly increased the level of GSH and decreased the level of MDA. Findings from both animal and studies suggest that ursolic acid decreases inflammatory cytokine levels, elevates antioxidant enzyme levels, and reduces oxidative stress levels (graphical abstract). This meta-analysis furnishes compelling evidence for the anti-inflammatory and antioxidant properties of ursolic acid.
PubMed: 37841938
DOI: 10.3389/fphar.2023.1256946 -
Human Reproduction Open 2023What is the role of iron in the pathophysiology of endometriosis?
STUDY QUESTION
What is the role of iron in the pathophysiology of endometriosis?
SUMMARY ANSWER
Iron excess is demonstrated wherever endometriotic tissues are found and is associated with oxidative stress, an inflammatory micro-environment, and cell damage; the iron-mediated oxidative stress is independently linked to subfertility, symptom severity, and malignant transformation.
WHAT IS KNOWN ALREADY
Iron is found in excess in endometriotic tissues, and multiple mechanisms have been studied and posited to explain this. It is clear that iron excess plays a vital role in promoting oxidative stress and cell damage. The evidence base is large, but no comprehensive reviews exist to summarize our understanding and highlight the overarching themes to further our understanding and suggest future directions of study for the field.
STUDY DESIGN SIZE DURATION
This systematic review with a thematic analysis retrieved studies from the PubMed, Embase, Web of Science, and Cochrane Library databases and searches were conducted from inception through to August 2022. Human and animal studies published in the English language were included and identified using a combination of exploded MeSH terms ('Iron' and 'Endometriosis') and free-text search terms ('Iron', 'Ferric', 'Ferrous', 'Endometriosis', 'Endometrioma').
PARTICIPANTS/MATERIALS SETTING METHODS
This review was reported in accordance with the PRISMA guidelines. All studies reporting original data concerning the role of iron or iron complexes in the pathophysiology of endometriosis were included. Studies that did not report original data or provided a review of the field were excluded. Bias analysis was completed for each included study by using the Newcastle-Ottawa scoring system.
MAIN RESULTS AND THE ROLE OF CHANCE
There were 776 records identified and these were screened down to 53 studies which met the eligibility criteria, including 6 animal and 47 human studies, with 3556 individual participants. Iron excess is demonstrated in various tissues and fluids, including ovarian endometriomas, ovarian follicles, ectopic endometriotic lesions, and peritoneal fluid. Markers of oxidative stress are strongly associated with high iron levels, and aberrant expression of iron-transport proteins has been demonstrated. Abnormal resistance to ferroptosis is likely. Iron-mediated oxidative stress is responsible for a pro-inflammatory micro-environment and is linked to subfertility, symptom severity, and, possibly, malignant transformation.
LIMITATIONS REASONS FOR CAUTION
A minority of the included studies were of objectively low quality with a high risk of bias and may lead to misleading conclusions. Additionally, multiple studies failed to appropriately characterize the included patients by known confounding variables, such as menstrual cycle phase, which may introduce bias to the findings.
WIDER IMPLICATIONS OF THE FINDINGS
Current literature depicts a central role of aberrant iron mechanics and subsequent oxidative stress in endometriosis. It is likely that iron excess is at least partly responsible for the persistence and proliferation of ectopic endometriotic lesions. As such, iron mechanics represent an attractive target for novel therapeutics, including iron chelators or effectors of the iron-oxidative stress pathway. There are significant gaps in our current understanding, and this review highlights and recommends several topics for further research. These include the role of iron chelation, resistance to ferroptosis, the relationship between iron excess and localized hypoxia, systemic iron pathophysiology in endometriosis, and the role of oxidative stress in malignant transformation.
STUDY FUNDING/COMPETING INTERESTS
J.W. and S.G.P. are supported by clinical fellowships at Liverpool University Hospital NHS Foundation trust. No additional funding was requested or required for the completion of this work. C.J.H. is supported by a Wellbeing of Women project grant (RG2137). D.K.H. is supported by a Wellbeing of Women project grant (RG2137) and an MRC clinical research training fellowship (MR/V007238/1). The authors have no conflicts of interest to declare.
REGISTRATION NUMBER
A protocol was prospectively registered with the PROSPERO database in August 2021 (CRD42021272818).
PubMed: 37638130
DOI: 10.1093/hropen/hoad033 -
Nutrients Aug 2023This paper presents a systematic review of studies investigating the effects of fatty acid supplementation in potentially preventing and treating sarcopenia. PubMed,... (Review)
Review
This paper presents a systematic review of studies investigating the effects of fatty acid supplementation in potentially preventing and treating sarcopenia. PubMed, Embase, and Web of Science databases were searched using the keywords 'fatty acid' and 'sarcopenia'. Results: A total of 14 clinical and 11 pre-clinical (including cell and animal studies) studies were included. Of the 14 clinical studies, 12 used omega-3 polyunsaturated fatty acids (PUFAs) as supplements, 1 study used ALA and 1 study used CLA. Seven studies combined the use of fatty acid with resistant exercises. Fatty acids were found to have a positive effect in eight studies and they had no significant outcome in six studies. The seven studies that incorporated exercise found that fatty acids had a better impact on elderlies. Four animal studies used novel fatty acids including eicosapentaenoic acid, trans-fatty acid, and olive leaf extraction as interventions. Three animal and four cell experiment studies revealed the possible mechanisms of how fatty acids affect muscles by improving regenerative capacity, reducing oxidative stress, mitochondrial and peroxisomal dysfunctions, and attenuating cell death. Conclusion: Fatty acids have proven their value in improving sarcopenia in pre-clinical experiments. However, current clinical studies show controversial results for its role on muscle, and thus the mechanisms need to be studied further. In the future, more well-designed randomized controlled trials are required to assess the effectiveness of using fatty acids in humans.
Topics: Animals; Humans; Muscles; Cell Death; Databases, Factual; Dietary Supplements; Eicosapentaenoic Acid; Fatty Acids; Sarcopenia
PubMed: 37630803
DOI: 10.3390/nu15163613 -
Iranian Journal of Public Health Dec 2023Working in hot environments can cause diseases and reduce performance by upsetting the balance of physiological parameters of workers' bodies. Bakers are among the... (Review)
Review
BACKGROUND
Working in hot environments can cause diseases and reduce performance by upsetting the balance of physiological parameters of workers' bodies. Bakers are among the people exposed to heat stress continuously and daily. This review study aimed to investigate the effect of heat stress on bakers.
METHODS
In this review study, the related articles based on keywords were reviewed using "IranMedex", "Science Direct", "PubMed", "Scopus", "Web of Science", "SID", "Google Scholar", and "Magiran" databases from the years 2000 to 2021. The used search terms were "Heat stress", "Heat strain", "Heat exposure", "Heat waves", "Workplace", "Baker", and "health effects". In order to extract the required data, all parts of the articles have been reviewed.
RESULTS
Out of the 16 studies reviewed in this study, 43.75% were cross-sectional, 25% were descriptive cross-sectional, and 31.25% were performed according to other study designs. In all of the studies, the WBGT index was used to assess ambient heat stress. In most studies, the mean exposure temperature was higher than the WBGT-ACGIH limit, especially among traditional bakery workers. The findings showed that exposure to thermal stress significantly affects some hematological parameters of blood, oxidative stress, heart rate, and body temperature.
CONCLUSION
The situation of heat stress in the bakery environment is worrying in terms of health and reduced productivity of employees. Therefore, it is essential to take the necessary preventive and control measures to reduce heat stress and the resulting strain.
PubMed: 38435770
DOI: 10.18502/ijph.v52i12.14314 -
Frontiers in Endocrinology 2023Male infertility is a multifaceted issue that has gained scientific interest due to its increasing rate. Studies have demonstrated that oxidative stress is involved in... (Meta-Analysis)
Meta-Analysis
Protective effects of melatonin against oxidative stress induced by metabolic disorders in the male reproductive system: a systematic review and meta-analysis of rodent models.
BACKGROUND
Male infertility is a multifaceted issue that has gained scientific interest due to its increasing rate. Studies have demonstrated that oxidative stress is involved in male infertility development. Furthermore, metabolic disorders, including obesity, diabetes, hypo- and hyperthyroidism, are risk factors for male infertility, and oxidative stress is believed to contribute to this association. Melatonin, functioning as an oxidative scavenger, may represent a promising therapeutic approach for the prevention and treatment of metabolic disorder-associated male infertility.
MATERIAL AND METHODS
We systematically searched three online databases (PubMed, Scopus, and Web of Science) for studies that evaluated the effects of melatonin therapy on metabolic disorders-induce infertility in male rodents. The favorable outcomes were histopathological parameters of testicular tissue, reproductive hormones, and markers of oxidative stress. Then, meta-analyses were done for each outcome. The results are reported as standardized mean difference (Cohen's d) and 95% confidence interval.
RESULTS
24 studies with 31 outcomes were included. Rats and mice were the subjects. Studies have employed obesity, diabetes, hypothyroidism, hyperthyroidism, hyperlipidemia, and food deprivation as metabolic disorders. To induce these disorders, a high-fat diet, high-fructose diet, leptin, streptozotocin, alloxan, carbimazole, and levothyroxine were used. The outcomes included histopathologic characteristics (abnormal sperm morphology, apoptotic cells, apoptotic index, Johnsen's testicular biopsy score, seminiferous epithelial height, tubular basement membrane thickness, tubular diameter, sperm count, and motility), weight-related measurements (absolute epididymis, testis, and body weight, body weight gain, epididymal adipose tissue weight, and relative testis to body weight), hormonal characteristics (androgen receptor expression, serum FSH, LH, and testosterone level), markers of oxidative stress (tissue and serum GPx and MDA activity, tissue CAT, GSH, and SOD activity), and exploratory outcomes (serum HDL, LDL, total cholesterol, triglyceride, and blood glucose level). The overall pooled effect sizes were statistically significant for all histopathological characteristics and some markers of oxidative stress.
CONCLUSIONS
Melatonin can reduce damage to male rodents' gonadal tissue and improve sperm count, motility, and morphology in metabolic diseases. Future clinical studies and randomized controlled trials are needed to evaluate the safety and effectiveness of melatonin for male infertility in patients with metabolic diseases.
Topics: Animals; Male; Mice; Rats; Body Weight; Diabetes Mellitus; Hyperthyroidism; Infertility, Male; Melatonin; Metabolic Diseases; Obesity; Oxidative Stress; Rodentia; Semen; Testis
PubMed: 37476491
DOI: 10.3389/fendo.2023.1202560 -
Frontiers in Pharmacology 2023Although several meta-analyses support the positive effect of coenzyme Q10 (CoQ10) on biomarkers of oxidative stress and inflammation, the results of some other studies...
Although several meta-analyses support the positive effect of coenzyme Q10 (CoQ10) on biomarkers of oxidative stress and inflammation, the results of some other studies reject such effects. Therefore, in this umbrella meta-analysis, we performed a comprehensive systematic search in such databases as Web of Science, PubMed, Scopus, Embase, and Google Scholar up to January 2023. Based on standardized mean difference analysis, CoQ10 supplementation significantly decreased serum C-reactive protein (CRP) (ES = -0.39; 95% CI: 0.77, -0.01, = 0.042) and malondialdehyde (MDA) (ES = -1.17; 95% CI: 1.55, -0.79, < 0.001), while it increased the total antioxidant capacity (TAC) (ES = 1.21; 95% CI: 0.61, 1.81, < 0.001) and serum superoxide dismutase (SOD) activity (ES = 1.08; 95% CI: 0.37, 1.79, = 0.003). However, CoQ10 supplementation had no significant reducing effect on tumor-necrosis factor-alpha (TNF- α) (ES = -0.70; 95% CI: 2.09, 0.68, = 0.320) and interleukin-6 (IL-6) levels (ES = -0.85; 95% CI: 1.71, 0.01, = 0.053). Based on weighted mean difference analysis, CoQ10 supplementation considerably decreased TNF-α (ES = -0.46, 95% CI: 0.65, -0.27; < 0.001), IL-6 (ES = -0.92, 95% CI: 1.40, -0.45; < 0.001), and CRP levels (effect sizes = -0.28, 95% CI: 0.47, -0.09; < 0.001). The results of our meta-analysis supported the alleviating effects of CoQ10 on markers of inflammation cautiously. However, CoQ10 had antioxidant effects regarding the improvement of all the studied antioxidant and oxidative stress biomarkers. https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=323861, identifier CRD42022323861.
PubMed: 37614320
DOI: 10.3389/fphar.2023.1191290 -
Journal of Pharmaceutical Analysis Dec 2023This review aims to identify in vivo studies investigating the potential of plant substances and their natural molecules in managing inflammatory bowel disease (IBD).... (Review)
Review
This review aims to identify in vivo studies investigating the potential of plant substances and their natural molecules in managing inflammatory bowel disease (IBD). Specifically, the objective is to examine the impact of these substances on interleukins and other key inflammatory signaling markers. Relevant articles published up to December 2022 were identified through a search of the PubMed, Scopus, Web of Science, and Embase databases. The search used keywords including "inflammatory bowel disease", "medicinal plants", "natural molecules", "anti-inflammatory", and "ulcerative colitis", and identified 1,878 potentially relevant articles, of which 89 were included in this review after completion of the selection process. This study provides preclinical data on natural products (NPs) that can potentially treat IBD, including ulcerative colitis. The main actions of these NPs relate to their effects on nuclear factor kappa B (NF-κB), the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway, the regulation of T helper 17/regulatory T cells balance, and oxidative stress. The ability of these NPs to inhibit intestinal inflammation appears to be dependent on lowering levels of the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-17, via the Jun N-terminal kinase (JNK)1, NF-κβ-p65, and STAT3 pathways. In addition, NPs were shown to reduce oxidative stress and the severity of ulcerative colitis, as well as increase the activity of antioxidant enzymes. These actions suggest that NPs represent a promising treatment for IBD, and potentially have greater efficacy and safety than current treatments.
PubMed: 38223446
DOI: 10.1016/j.jpha.2023.09.012 -
Eco-Environment & Health Dec 2023Micro- and nano-plastics (MNPs) pollution has become a pressing global environmental issue, with growing concerns regarding its impact on human health. However, evidence... (Review)
Review
Micro- and nano-plastics (MNPs) pollution has become a pressing global environmental issue, with growing concerns regarding its impact on human health. However, evidence on the effects of MNPs on human health remains limited. This paper reviews the three routes of human exposure to MNPs, which include ingestion, inhalation, and dermal contact. It further discusses the potential routes of translocation of MNPs in human lungs, intestines, and skin, analyses the potential impact of MNPs on the homeostasis of human organ systems, and provides an outlook on future research priorities for MNPs in human health. There is growing evidence that MNPs are present in human tissues or fluids. Lab studies, including animal models and human-derived cell cultures, revealed that MNPs exposure could negatively affect human health. MNPs exposure could cause oxidative stress, cytotoxicity, disruption of internal barriers like the intestinal, the air-blood and the placental barrier, tissue damage, as well as immune homeostasis imbalance, endocrine disruption, and reproductive and developmental toxicity. Limitedly available epidemiological studies suggest that disorders like lung nodules, asthma, and blood thrombus might be caused or exacerbated by MNPs exposure. However, direct evidence for the effects of MNPs on human health is still scarce, and future research in this area is needed to provide quantitative support for assessing the risk of MNPs to human health.
PubMed: 38435355
DOI: 10.1016/j.eehl.2023.08.002