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1.
Sci Total Environ ; 933: 173032, 2024 Jul 10.
Article in English | MEDLINE | ID: mdl-38734099

ABSTRACT

Ferroptosis is frequently observed in fibrosis and diseases related to iron metabolism disorders in various mammalian organs. However, research regarding the damage mechanism of ferroptosis in the female reproductive system of avian species remains unclear. In this study, Muscovy female ducks were divided into three groups which were given purified water, 1 mg/L polyvinyl chloride microplastics (PVC-MPs) and 10 mg/L PVC-MPs for two months respectively, to investigate the ferroptosis induced by PVC-MPs caused ovarian tissue fibrosis that lead to premature ovarian failure. The results showed that the high accumulation of PVC-MPs in ovarian tissue affected the morphology and functional activity of ovarian granulosa cells (GCs) and subsequently caused the follicular development disorders and down-regulated the immunosignaling of ovarian steroidogenesis proteins 3ß-hydroxysteroid dehydrogenase (3ß-HSD), 17ß-hydroxysteroid dehydrogenase (17ß-HSD), CYP11A1 cytochrome (P450-11A1) and CYP17A1 cytochrome (P450-17A1) suggested impaired ovarian function. In addition, PVC-MPs significantly up-regulated positive expression of collagen fibers, significantly increased lipid peroxidation and malondialdehyde (MDA) level, along with encouraged overload of iron contents in the ovarian tissue were the characteristics of ferroptosis. Further, immunohistochemistry results confirmed that immunosignaling of ferroptosis related proteins Acyl-CoA synthetase (ACSL4), Cyclooxygenase 2 (COX2) and ferritin heavy chain 1 (FTH1) were significantly increased, but solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase (GPX4) were decreased by PVC-MPs in the ovarian tissue. In conclusion, our study demonstrates that PVC-MPs induced ferroptosis in the ovarian GCs, leading to follicle development disorders and ovarian tissue fibrosis, and ultimately contributing to various female reproductive disorders through regulating the proteins expression of ferroptosis.


Subject(s)
Ducks , Ferroptosis , Microplastics , Ovary , Polyvinyl Chloride , Animals , Female , Ferroptosis/drug effects , Polyvinyl Chloride/toxicity , Ovary/drug effects , Microplastics/toxicity , Water Pollutants, Chemical/toxicity , Granulosa Cells/drug effects , Granulosa Cells/metabolism
2.
Chem Biol Interact ; 394: 110976, 2024 May 01.
Article in English | MEDLINE | ID: mdl-38552764

ABSTRACT

It is widely accepted that humans are constantly exposed to micro-plastics and nano-plastics through various routes, including inhalation of airborne particles, exposure to dust, and consumption of food and water. It is estimated that humans may consume thousand to millions of micro-plastic particles, equating to several milligrams per day. Prolonged exposure to micro-plastics and nano-plastics has been linked to negative effects on different living organisms, including neurotoxicity, gastrointestinal toxicity, nephrotoxicity, and hepatotoxicity, and developmental toxicities. The main purpose of this review is to explore the effect of micro-plastics and nano-plastics on the male and female reproductive system, as well as their offspring, and the associated mechanism implicated in the reproductive and developmental toxicities. Micro-plastics and nano-plastics have been shown to exert negative effects on the reproductive system of both male and female mammals and aquatic animals, including developmental impacts on gonads, gametes, embryo, and their subsequent generation. In addition, micro-plastics and nano-plastics impact the hypothalamic-pituitary axes, leading to oxidative stress, reproductive toxicity, neurotoxicity, cytotoxicity, developmental abnormalities, poor sperm quality, diminishes ovarian ovulation and immune toxicity. This study discusses the so many different signaling pathways associated in the male and female reproductive and developmental toxicity induced by micro-plastics and nano-plastics.


Subject(s)
Reproduction , Signal Transduction , Female , Animals , Male , Reproduction/drug effects , Signal Transduction/drug effects , Humans , Microplastics/toxicity , Nanoparticles/toxicity
3.
PLoS One ; 8(7): e69066, 2013.
Article in English | MEDLINE | ID: mdl-23894407

ABSTRACT

Neonatal rat primary myocardial cells were subjected to heat stress in vitro, as a model for investigating the distribution and expression of Hsp27 and αB-crystallin. After exposure to heat stress at 42°C for different durations, the activities of enzymes expressed during cell damage increased in the supernatant of the heat-stressed myocardial cells from 10 min, and the pathological lesions were characterized by karyopyknosis and acute degeneration. Thus, cell damage was induced at the onset of heat stress. Immunofluorescence analysis showed stronger positive signals for both Hsp27 and αB-crystallin from 10 min to 240 min of exposure compared to the control cells. According to the Western blotting results, during the 480 min of heat stress, no significant variation was found in Hsp27 and αB-crystallin expression; however, significant differences were found in the induction of their corresponding mRNAs. The expression of these small heat shock proteins (sHsps) was probably delayed or overtaxed due to the rapid consumption of sHsps in myocardial cells at the onset of heat stress. Our findings indicate that Hsp27 and αB-crystallin do play a role in the response of cardiac cells to heat stress, but the details of their function remain to be investigated.


Subject(s)
HSP27 Heat-Shock Proteins/metabolism , Hot Temperature , Myocytes, Cardiac/metabolism , Stress, Physiological , alpha-Crystallin B Chain/metabolism , Animals , Creatine Kinase, MB Form/metabolism , Enzyme Activation , Gene Expression , Gene Expression Regulation , HSP27 Heat-Shock Proteins/genetics , Myocytes, Cardiac/enzymology , Myocytes, Cardiac/pathology , Protein Transport , RNA, Messenger/genetics , Rats , alpha-Crystallin B Chain/genetics
4.
Article in English | WPRIM (Western Pacific) | ID: wpr-65168

ABSTRACT

The aim of this study was to assess changes of Hsp70 and HSF-1 protein and mRNA expression in stress-sensitive organs of pigs during transportation for various periods of time. Twenty pigs were randomly divided into four groups (0 h, 1 h, 2 h, and 4 h of transportation). A significant increased activity of AST and CK was observed after 1 h and 2 h of transportation. Histopathological changes in the heart, liver, and stomach indicated that these organs sustained different degrees of injury. Hsp70 protein expression in the heart and liver of transported pigs did not change significantly while it increased significantly (p < 0.05) in the stomach. Hsp70 mRNA levels decreased significantly (p < 0.05) in the heart after 4 h of transportation. However, mRNA expression increased significantly in the liver after 1 (p < 0.05) and 4 h (p < 0.01) of transportation, and increased significantly in the stomach of the transported pigs after 1, 4 (p < 0.01), and 2 h (p < 0.05). HSF-1 levels were reduced at 1 and 4 h (p < 0.05) only in the hearts of transported pigs. These results indicate that Hsp70 mediates distinct stress-related functions in different tissues during transportation.


Subject(s)
Animals , Creatine Kinase/blood , DNA-Binding Proteins/metabolism , Enzyme-Linked Immunosorbent Assay/veterinary , HSP70 Heat-Shock Proteins/metabolism , Liver/metabolism , Myocardium/metabolism , RNA, Messenger/metabolism , Random Allocation , Real-Time Polymerase Chain Reaction/veterinary , Stomach/metabolism , Stress, Physiological , Swine/blood , Time Factors , Transaminases/blood , Transcription Factors/metabolism , Transportation
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