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•Polystyrene microplastics could enter into the ovary of rat.•Polystyrene microplastics cause ovary fibrosis via Wnt/β-Catenin signaling pathway.•Polystyrene microplastics cause ...granulosa cells apoptosis of ovary.•Polystyrene microplastics could result in decrease of ovarian reserve capacity.
Microplastics (MPs) are receiving increased attention as a harmful environmental pollutant. Studies have investigated that MPs have reproductive toxicity, but the mechanism is little known. Here, we aimed to investigate the effects of polystyrene microplastics (PS-MPs) on ovary in rats and the underlying molecular mechanisms. in vivo, thirty-two female Wistar rats were exposed to 0.5 μm PS-MPs at different concentrations (0, 0.015, 0.15 and 1.5 mg/d) for 90 days. And then, all animals were sacrificed, ovaries and blood were collected for testing. in vitro, granulosa cells (GCs) were separated from rat ovary and treated with 0、1、5、25 μg/mL PS-MPs and reactive oxygen species (ROS) inhibitor N-Acetyl-l-cysteine (NAC) respectively. Our results showed that PS-MPs could enter into GCs and result in the reducing of growing follicles number. And the Enzyme-linked immunosorbent assay (ELISA) manifested that PS-MPs could obviously decrease the level of anti-Müllerian hormone (AMH). In addition, PS-MPs induced oxidative stress, apoptosis of GCs and ovary fibrosis evidenced by assay kits, flow cytometry, immunohistochemistry, Masson’s trichrome and Sirius red staining. Moreover, the western blot assay manifested that PS-MPs exposure significantly increased the expression levels of Wnt/β-Catenin signaling pathways-related proteins (Wnt, β-catenin, p-β-catenin) and the main fibrosis markers (transforming growth factor-β (TGF-β), fibronectin, α-smooth muscle actin (α-SMA). Additionally, the expression levels of Wnt and p-β-catenin, apoptosis of GCs decreased after NAC treatment. In summary, polystyrene microplastics cause fibrosis via Wnt/β-Catenin signaling pathway activation and granulosa cells apoptosis of ovary through oxidative stress in rats, both of which ultimately resulted in decrease of ovarian reserve capacity.
This randomized clinical trial aimed to determine the extent to which injectable micronutrient supplementation at birth can improve intranasal vaccine response by ameliorating oxidative stress in ...dairy calves from birth to weaning. For this, 120 Holstein heifer calves were enrolled at birth and randomly allocated into one of 4 groups. The 4 groups included 3 commercially available micronutrient supplements (Selenium, Copper, Zinc, and Manganese; Selenium & Vitamin E; and Vitamins E, A, and D) and one control (saline). Calves received an intranasal vaccine against the respiratory viruses parainfluenza 3, bovine herpesvirus type 1 (BHV-1), and bovine respiratory syncytial virus (BRSV) within the first wk of life. Weight (BW) and hip height (HH) were recorded, and a blood sample and nasal secretion sample were collected at birth before treatment and vaccine administration as well as weekly until weaning at 8 wk. Health scores, including thoracic ultrasound assessment, were recorded weekly from wk 1 to wk 8. Farm treatment records were collected after the completion of the study. Serum micronutrient concentrations were determined from birth to weaning to identify micronutrient status, and serum blood metabolites were analyzed as markers of nutrient utilization. Redox balance was determined in serum as a ratio of reactive oxygen and nitrogen species (RONS) to antioxidant capacity (AOP), known as the oxidant status index (OSi). Intranasal vaccine response was quantified as anti-BRSV and anti-BHV-1 immunoglobulin A (IgA) concentrations in nasal secretions. Linear mixed models with repeated measures were built for the following outcome variables: micronutrient concentrations, blood metabolites, redox balance, IgA concentrations, BW, and HH. Pre-planned contrasts of control vs supplemented were also built for the primary outcome of IgA concentrations. A logistic regression mixed model was built for health events and treatment of disease. Serum selenium concentrations were greater in calves receiving supplements containing Se throughout the first 4 wk of life. However, we did not observe any consistent differences in the other micronutrients. The metabolic biomarkers indicate that supplemented calves had better energy status, as suggested by lower BHB and nonesterified fatty acids (NEFA) concentrations. Supplemented calves showed improved redox balance, as indicated by lower OSi throughout the first wk of life. Calves supplemented with antioxidants at birth had higher anti-BRSV IgA than control calves. Our results indicate an improved immune response to vaccines in calves supplemented with antioxidants at birth. However, this did not translate to growth and health performance as there were no differences in average daily gain (ADG) or incidence of health events throughout the pre-weaning period. This study provides evidence that improving the antioxidant capacity might improve vaccine response, and further research is required to investigate the appropriate frequency and dose of supplementation to improve calf growth and health.
Purpose of Review
Atherosclerosis is now considered a chronic inflammatory disease. Oxidative stress induced by generation of excess reactive oxygen species has emerged as a critical, final common ...mechanism in atherosclerosis. Reactive oxygen species (ROS) are a group of small reactive molecules that play critical roles in the regulation of various cell functions and biological processes. Although essential for vascular homeostasis, uncontrolled production of ROS is implicated in vascular injury. Endogenous anti-oxidants function as checkpoints to avoid these untoward consequences of ROS, and an imbalance in the oxidant/anti-oxidant mechanisms leads to a state of oxidative stress. In this review, we discuss the role of ROS and anti-oxidant mechanisms in the development and progression of atherosclerosis, the role of oxidized low-density lipoprotein cholesterol, and highlight potential anti-oxidant therapeutic strategies relevant to atherosclerosis.
Recent Findings
There is growing evidence on how traditional risk factors translate into oxidative stress and contribute to atherosclerosis. Clinical trials evaluating anti-oxidant supplements had failed to improve atherosclerosis. Current studies focus on newer ROS scavengers that specifically target mitochondrial ROS, newer nanotechnology-based drug delivery systems, gene therapies, and anti-miRNAs. Synthetic LOX-1 modulators that inhibit the effects of Ox-LDL are currently in development.
Summary
Research over the past few decades has led to identification of multiple ROS generating systems that could potentially be modulated in atherosclerosis. Therapeutic approaches currently being used for atheroslcerotic vascular disease such as aspirin, statins, and renin-angiotensin system inhibitors exert a pleiotropic antioxidative effects. There is ongoing research to identify novel therapeutic modalities to selectively target oxidative stress in atherosclerosis.
The existence of free radicals in living cells was first reported in 1954 and this important finding helped launch the field of free radical biology. However, the discovery that muscular exercise is ...associated with increased biomarkers of oxidative stress did not occur until 1978. Following the initial report that exercise promotes oxidative stress in humans, many studies have confirmed that prolonged or short‐duration high intensity exercise results in increased radical production in active skeletal muscles resulting in the formation of oxidized lipids and proteins in the working muscles. Since these early descriptive studies, the investigation of radicals and redox biology related to exercise and skeletal muscle has grown as a discipline and the importance of this research in the biomedical sciences is widely recognized. This review will briefly summarize the history of research in exercise‐induced oxidative stress and will discuss the major paradigm shifts that the field has undergone and continues to experience. We conclude with a discussion of future directions in the hope of stimulating additional research in this important field.
Diabetes mellitus (DM) is the major cause of end-stage renal disease (ESRD) globally, and novel treatments are urgently needed. Current therapeutic approaches for diabetic nephropathy (DN) are ...focussing on blood pressure control with inhibitors of the renin–angiotensin–aldosterone system, on glycaemic and lipid control, and life-style changes. In this review, we highlight new molecular insights aiding our understanding of the initiation and progression of DN, including glomerular insulin resistance, dysregulation of cellular substrate utilisation, podocyte–endothelial communication, and inhibition of tubular sodium coupled glucose reabsorption. We believe that these mechanisms offer new therapeutic targets that can be exploited to develop important renoprotective treatments for DN over the next decade.
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