Oxidative stress biomarkers in pregnancy: a systematic review.

BACKGROUND: This systematic review explores the level of oxidative stress (OS) markers during pregnancy and their correlation with complications. Unlike previous studies, it refrains from directly investigating the role of OS but instead synthesises data on the levels of these markers and their implications for various pregnancy-related complications such as preeclampsia, intrauterine growth restrictions, preterm premature rupture of membranes, preterm labour, gestational diabetes mellitus and miscarriages. METHOD: STUDY DESIGN: Utilizing a systematic review approach, we conducted a comprehensive search across databases, including MEDLINE, CINAHL (EBSCOhost), ScienceDirect, Web of Science, and SCOPUS. Our search encompassed all publication years in English. RESULTS: After evaluating 54,173 records, 45 studies with a low risk of bias were selected for inclusion. This systematic review has underscored the importance of these markers in both physiological and pathological pregnancy states such as preeclampsia, intrauterine growth restrictions, preterm premature rupture of membranes, preterm labour, gestational diabetes mellitus and miscarriages. CONCLUSION: This systematic review provides valuable insights into the role of OS in pregnancy and their connection to complications. These selected studies delved deeply into OS markers during pregnancy and their implications for associated complications. The comprehensive findings highlighted the significance of OS markers in both normal and pathological pregnancy conditions, paving the way for further research in this field.

Etlingera elatior Flower Aqueous Extract Protects against Oxidative Stress-Induced Nephropathy in a Rat Model of Type 2 Diabetes.

Diabetes mellitus (DM) is a known systemic disease with increasing global prevalence and multi-organ complications including diabetic nephropathy (DN). The trend of using medicinal plants in the management of DM is increasing exponentially. Etlingera elatior is a medicinal plant that contains chemicals and antioxidants that delay the oxidation process. However, available data focusing on its use on DN are inconsistent and scarce. This study aims to investigate the antidiabetic and nephroprotective effects of E. elatior flower aqueous extract (EEAE) in a type 2 DM rat (T2DR) model. The T2DR model was developed using a combination of a high-fat diet (HFD) and a low dose of streptozotocin (STZ) at 35 mg/kg. Thirty-two Sprague Dawley male rats were randomly divided into four groups (n = 8): (1) control (normal rat), (2) T2DR (untreated-type 2 diabetic rat), (3) Met (250 mg/kg metformin-treated T2DR), and (4) EEAE (1000 mg/kg EEAE-treated T2DR). All treatments were administered orally for 6 weeks. EEAE significantly reduced fasting blood glucose (FBG), microalbuminuria, serum creatinine, and serum blood urea nitrogen. EEAE also reduced malondialdehyde (MDA) and enhanced the levels of antioxidant markers-superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and total antioxidant capacity (T-AOC). The inflammatory marker (interleukin (IL)-6) and fibrosis markers (transforming growth factor-beta (TGF-ß), and connective tissue growth factor (CTGF)) were significantly decreased in the EEAE-treated group. The T2DR group developed DN, which was characterized by segmental sclerosis of the glomeruli associated with focal tubular atrophy and interstitial fibrosis. Interestingly, the histology of kidney tissue in the EEAE group was preserved. This effect was similar to that of the control drug metformin. In summary, the antidiabetic and nephroprotective effects might be related to the antioxidant properties and anti-inflammatory effects of the EEAE. The antidiabetic activity could be due to the presence of the active compound cyanidin-3-O-glycosides, which is an anthocyanin antioxidant, that is present in the EEAE. E. elatior has the potential to be developed as a natural source of antioxidants that can be used for the prevention or even the treatment of DM. These findings could lead to future research into the therapeutic use of E. elatior in alleviating the progression of DM and thus preventing nephropathy.

Current Updates on Potential Role of Flavonoids in Hypoxia/Reoxygenation Cardiac Injury Model.

Clinically, timely reperfusion strategies to re-establish oxygenated blood flow in ischemic heart diseases seem to salvage viable myocardium effectively. Despite the remarkable improvement in cardiac function, reperfusion therapy could paradoxically trigger hypoxic cellular injury and dysfunction. Experimental laboratory models have been developed over the years to explain better the pathophysiology of cardiac ischemia-reperfusion injury, including the in vitro hypoxia-reoxygenation cardiac injury model. Furthermore, the use of nutritional myocardial conditioning techniques have been successful. The cardioprotective potential of flavonoids have been greatly linked to its anti-oxidant, anti-apoptotic and anti-inflammatory properties. While several studies have reviewed the cardioprotective properties of flavonoids, there is a scarce evidence of their function in the hypoxia-reoxygenation injury cell culture model. Hence, the aim of this review was to lay out and summarize our current understanding of flavonoids' function in mitigating hypoxia-reoxygenation cardiac injury based on evidence from the last five years. We also discussed the possible mechanisms of flavonoids in modulating the cardioprotective effects as such information would provide invaluable insight on future therapeutic application of flavonoids.

Lipid peroxidation in the descending thoracic aorta of rats deprived of REM sleep using the inverted flowerpot technique.

NEW FINDINGS: What is the central question of this study? Deprivation of rapid eye movement (REM) sleep is associated with increased oxidative stress, but its effects on the blood vessels are poorly documented. We investigated whether REM sleep deprivation induces oxidative stress and causes lipid peroxidation in the aorta. What is the main finding and its important? We demonstrate that REM sleep deprivation induces oxidative stress and mediates lipid peroxidation in the aorta. This can cause endothelial changes and increased blood pressure. These findings will contribute to the growing body of literature on the mechanism underlying the effects of sleep deprivation on cardiovascular disease. ABSTRACT: Oxidative stress-mediated lipid peroxidation is a known cause of endothelial injury or dysfunction. Deprivation of rapid eye movement (REM) sleep is associated with oxidative stress. To date, the pathogenesis of increased blood pressure after sleep deprivation remains poorly understood, particularly in the REM sleep phase. Our aim was to investigate the effects of REM sleep deprivation on blood vessels in the REM sleep-deprived rat model. Twenty-eight male Sprague-Dawley rats were divided into four equal groups: free-moving control rats, rats deprived of REM sleep for 72 h (REMsd), tank control rats and 72 h sleep-recovered rats after 72 h of REM sleep deprivation. The rats were deprived of REM sleep using the inverted flowerpot technique. Food consumption, body weight gain and systolic blood pressure were monitored. At the end of the experiment, the descending thoracic aorta was isolated for the measurement of oxidative stress markers. Despite a significant increase in food consumption in the REMsd group compared with the other groups, there was a significant reduction in body weight gain. Systolic blood pressure also showed a significant increase in the REMsd group compared with the other groups. Superoxide dismutase activity was significantly lower and malondialdehyde concentrations significantly higher in the REMsd group compared with the other groups. Increased levels of malondialdehyde are suggestive of lipid peroxidation in the blood vessels, and oxidative stress may be attributed to the initiation of the process. The changes after REM sleep deprivation revert during sleep recovery. In conclusion, the findings of the present study provide convincing evidence that REM sleep deprivation induced lipid peroxidation, leading to endothelial damage.

Phenolic Compounds and the Anti-Atherogenic Effect of Bee Bread in High-Fat Diet-Induced Obese Rats.

This study was undertaken to determine the phenolic compounds and the anti-atherogenic effect of bee bread in high-fat diet (HFD)-induced obese rats. The presence of phenolic compounds in bee bread was determined by liquid chromatography-mass spectrometry. Thirty-two male Sprague Dawley rats were divided into four groups, (n = 8/group); i.e., Normal (N), HFD (high-fat diet), HFD + BB (high-fat diet and 0.5 g/kg/day bee bread), and HFD + O (high-fat diet and 10 mg/kg/day orlistat) groups. After 6 weeks of the experiment, rats were sacrificed. Five phenolic compounds were identified in bee bread; namely, caffeic acid, ferulic acid, kaempferol, apigenin, and isorhamnetin. Bee bread significantly reduced Lee obesity index and levels of total cholesterol (TC), low-density lipoprotein (LDL), fatty acid synthase (FAS) activity, atherogenic index, oxidised-LDL (oxLDL), and malondialdehyde (MDA), and significantly increased aortic antioxidant activities, such as those of superoxide dismutase (SOD) and glutathione peroxidase (GPx). Adipocyte sizes were found to be smaller in the HFD + BB group compared to the N group, and en face aortas showed an absence of atherosclerotic plaque in rats supplemented with bee bread. These changes might suggest an anti-atherogenic effect of bee bread in HFD-induced obese rats via its antioxidant and hypocholesterolaemic properties.

Pyruvate reduces in vitro the embryotoxic effect of peritoneal fluid from infertile women with endometriosis.

OBJECTIVES: To ascertain the embryotoxicity of peritoneal fluid from infertile women with endometriosis (PF-E), on mouse embryos in culture and to examine the effect of pyruvate in the culture medium on PF-E induced embryotoxicity. STUDY DESIGN: Blood-free peritoneal fluid samples were obtained during laparoscopic investigation for infertility from 21 infertile women with endometriosis. The severity of endometriosis ranged from minimal or mild (PF-min to mild-E; n=7), moderate (PF-mod-E; n=7), to severe (PF-sev-E; n=7). Peritoneal fluid samples were centrifuged at 600 x g for 10 min and 4 degrees C, and the supernatant was incubated at 56 degrees C for 30 min in a water bath to inactivate the complement protein. Mice were super ovulated with intraperitoneal injection (IP) of 5IU of pregnant mare serum gonadotrophin and human chorion gonadotrophin. Twenty-four hours after confirmation of mating two-cell mouse embryos were obtained. They were then cultured in modified Whitten's medium (mWM) with peritoneal fluid from patients with endometriosis, and either in the absence or presence of excess pyruvate (0.062 mmol(-1)). Embryos were cultured for 72 h. RESULTS AND CONCLUSION: Addition of 5% PF-E significantly (p<0.001) suppressed embryo growth at 24, 48, and 72 h of culture and the degree of suppression correlated with the severity of the disease. The presence of 0.062 mmol(-1) pyruvate in the culture medium significantly (p<0.001) reduced the embryotoxicity of PF-min to mild-E and PF-mod-E at each stage of development, but was only seen at 24h of culture (p<0.001) in cultures with PF-sev-E even when the concentration of pyruvate in the medium was increased to 0.31 mmol(-1). This study confirms the embryotoxicity of PF-E in vitro, which was reduced by the presence pyruvate in the culture medium, particularly in cultures containing fluid from women with endometriosis of minimum or mild to moderate severity.