TBHP-induced oxidative stress alters microRNAs expression in mouse testis

Fatemi, Nayeralsadat; Sanati, Mohammad Hossein; Shamsara, Mehdi; Moayer, Fariborz; Zavarehei, M Jamali; Pouya, Alireza; Sayyahpour, ForoughAzam; Ayat, Hoda; Gourabi, Hamid

doi:10.1007/s10815-014-0302-4

Cited by 37 publications

(22 citation statements)

References 51 publications

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“…However, we cannot exclude the possibility that some of the damage observed in the sperm DNA may occur during the formation of spermatozoa in the testis. The oxidative stress generated by t-BHP altered the expression of miRNAs involved in the antioxidant response and spermatogenesis in mouse testis [41]. Although we did not see significant changes in spermatogenesis and the antioxidant response appears to be intact in rat testis, there is a possibility for the disruption of molecular mechanisms driven by miRNAs or epigenetic changes that can be associated with the permanent sperm DNA damage observed in this study.…”

Section: Discussioncontrasting

confidence: 60%

Long-Term Adverse Effects of Oxidative Stress on Rat Epididymis and Spermatozoa

Scarlata

O’Flaherty

2020

Antioxidants

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Oxidative stress is a common culprit of several conditions associated with male fertility. High levels of reactive oxygen species (ROS) promote impairment of sperm quality mainly by decreasing motility and increasing the levels of DNA oxidation. Oxidative stress is a common feature of environmental pollutants, chemotherapy and other chemicals, smoke, toxins, radiation, and diseases that can have negative effects on fertility. Peroxiredoxins (PRDXs) are antioxidant enzymes associated with the protection of mammalian spermatozoa against oxidative stress and the regulation of sperm viability and capacitation. In the present study, we aimed to determine the long-term effects of oxidative stress in the testis, epididymis and spermatozoa using the rat model. Adult male rats were treated with tert-butyl hydroperoxide (t-BHP) or saline (control group), and reproductive organs and spermatozoa were collected at 3, 6, and 9 weeks after the end of treatment. We determined sperm DNA oxidation and motility, and levels of lipid peroxidation and protein expression of antioxidant enzymes in epididymis and testis. We observed that cauda epididymal spermatozoa displayed low motility and high DNA oxidation levels at all times. Lipid peroxidation was higher in caput and cauda epididymis of treated rats at 3 and 6 weeks but was similar to control levels at 9 weeks. PRDX6 was upregulated in the epididymis due to t-BHP; PRDX1 and catalase, although not significant, followed similar trend of increase. Testis of treated rats did not show signs of oxidative stress nor upregulation of antioxidant enzymes. We concluded that t-BHP-dependent oxidative stress promoted long-term changes in the epididymis and maturing spermatozoa that result in the impairment of sperm quality.

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Section: Discussioncontrasting

confidence: 60%

Long-Term Adverse Effects of Oxidative Stress on Rat Epididymis and Spermatozoa

Scarlata

O’Flaherty

2020

Antioxidants

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“…miR-29 may serve tumor-suppressive and tumorigenic roles in cancer; thus, the expression of miR-29 may depend on the tissue and cellular context (30). It has been reported that RIPC protects the ischemic tissue from IR injury via a reactive oxygen species (ROS)-dependent pathway (11,31,32), and that oxidative stress alters miRNA expression (33,34). In the present study, oxidative stress or ROS were not measured.…”

Section: Discussionmentioning

confidence: 78%

MicroRNA-29a/b/c targets iNOS and is involved in protective remote ischemic preconditioning in an ischemia-reperfusion rat model of non-alcoholic fatty liver disease

et al. 2017

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Abstract. Remote ischemic preconditioning (RIPC) protects against the injury that is incurred by ischemia and reperfusion (IR); however, the role of RIPC in liver IR injury in non-alcoholic fatty liver disease (NAFLD) remains unclear. In this study, a NAFLD rat model was utilized in a series of different surgical procedures and molecular experiments. Rats of the IR group and the RIPC+IR group exhibited more severe injury than NAFLD control rats (in which the liver was prodded following a median-incision laparotomy). The liver condition, measured by serum alanine transaminase and aspartate transaminase levels, of the RIPC+IR group was better than that of the IR group. In addition, alanine transaminase and aspartate transaminase levels were lower in the RIPC+IR group compared with the IR group (P<0.001). Flow cytometry revealed that the cell apoptosis ratio was significantly lower in the RIPC+IR group than in the IR group (P<0.001). Reverse transcription-polymerase chain reaction (RT-qPCR) was used to assess miR-29a/b/c levels, revealing that they were significantly reduced in the RIPC and RIPC+IR groups, but did not vary in the IR group compared with the control group. RT-qPCR also revealed that iNOS mRNA levels were not significantly different among any of the NAFLD groups; however, western blot analysis indicated that iNOS protein levels were increased in the RIPC group and the RIPC+IR group compared with the control and IR groups. A luciferase reporter assay demonstrated that transfection with miR-29a/b/c mimics significantly decreased the luciferase activities of plasmids containing the wild-type iNOS 3'-untranslated region (UTR) (relative fluorescence intensity: 0.47±0.06 for miR-29a, 0.36±0.07 for miR-29b, 0.41±0.04 for miR-29c; P<0.001), whereas the activities of plasmids containing the mutant iNOS 3'-UTR sequence were not markedly affected [relative fluorescence intensity: 0.99±0.08 for miR-29a (P=0.1349), 0.99±0.09 for miR-29b (P= 0.1607), 0.97±0.07 for miR-29c (P= 0.1824)]. This suggested that miR-29a/b/c downregulates iNOS by directly targeting its 3'-UTR. In summary, the results suggest that RIPC has a protective effect in NAFLD liver IR injury, which may be due to reduced miR-29a/b/c levels in the skeletal muscle, leading to increased iNOS and, therefore, nitric oxide.

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“…After incubation of the homogenates with 20 µM DCFH-DA in dark at 37°C for 45 min, tissue homogenates were washed with PBS. Then, DCF fluorescence (green) was detected in the FL-1 channel using a BD FACScan flow cytometer (Becton Dickinson, San Jose, CA, USA) (21).…”

Section: Ros Assaymentioning

confidence: 99%

Maternal separation stress experienced by parents affects ovarian function in first generation of mice

Khodamoradi

Khosravizadeh

Amini-Khoei

et al. 2020

Preprint

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The maternal separation stress during postnatal development can adversely affect one's adulthood. Some parents' experiences may not only affect the phenotype of parents but also alter the reaction to environmental impacts in the offspring. The aim of this study is to investigate consequences of maternal separation stress in female first generation of mice whose parents were exposed to maternal separation stress. Maternal separation in pups was performed during post-natal days (PND) 2 to 14. Then, female pups of the first-generation were used in present study. The histological changes in ovaries, ROS production (using DCFH-DA assay), mRNA expression of NLRP3, ASC, caspase-1, TLR4, BAX, BCL2 and TNFα genes (using RT-PCR), levels of IL-18, IL-1β, ATP and GPx (using ELISA) and also protein expression of caspase-3 and NLRP3 (using immunocytochemistry) were assessed. Our findings showed that maternal separation stress experienced by parents significantly affects the numbers of primordial and primary follicles. Furthermore, ROS production increased and concentrations of ATP and GPx reduced in the first generation. Also, expression of cytokines and genes involved in inflammation and apoptosis including NLRP3, caspase-1, TLR4, TNFα, IL-1β, IL-18 and BCL2 were significantly affected in the first generation. Our results also showed that this stress significantly increased percentage of caspase-3 and NLRP3 positive cells in the ovarian tissue of the first generation. Our findings suggest that maternal separation stress experienced by parents may influence activation of inflammatory response in the ovarian tissue of their first generation which may induce apoptosis and consequently disturb folliculogenesis process.

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TBHP-induced oxidative stress alters microRNAs expression in mouse testis

Cited by 37 publications

References 51 publications

Long-Term Adverse Effects of Oxidative Stress on Rat Epididymis and Spermatozoa

Long-Term Adverse Effects of Oxidative Stress on Rat Epididymis and Spermatozoa

MicroRNA-29a/b/c targets iNOS and is involved in protective remote ischemic preconditioning in an ischemia-reperfusion rat model of non-alcoholic fatty liver disease

Maternal separation stress experienced by parents affects ovarian function in first generation of mice

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