The Experts below are selected from a list of 312 Experts worldwide ranked by ideXlab platform

C. Yan Cheng - One of the best experts on this subject based on the ideXlab platform.

  • Microtubule Cytoskeleton and Spermatogenesis-Lesson From Studies of Toxicant Models.
    Toxicological sciences : an official journal of the Society of Toxicology, 2020
    Co-Authors: Lingling Wang, Chris K.c. Wong, Ming Yan, Baiping Mao, Fei Sun, C. Yan Cheng
    Abstract:

    Studies have shown that mammalian testes, in particular the Sertoli cells, are highly susceptible to exposure of environmental toxicants, such as cadmium, perfluorooctanesulfonate, phthalates, 2,5-hexanedione and bisphenol A. However, important studies conducted by reproductive toxicologists and/or biologists in the past have been treated as toxicology reports per se. Yet, many of these studies provided important mechanistic insights on the toxicant-induced Testis Injury and reproductive dysfunction, relevant to the biology of the Testis and spermatogenesis. Furthermore, recent studies have shown that findings obtained from toxicant models are exceedingly helpful tools to unravel the biology of Testis function in particular spermatogenesis, including specific cellular events associated with spermatid transport to support spermiogenesis and spermiation. In this review, we critically evaluate some recent data, focusing primarily on the molecular structure and role of microtubules in cellular function, illustrating the importance of toxicant models to unravel the biology of microtubule cytoskeleton in supporting spermatogenesis, well beyond information on toxicology. These findings have opened up some potential areas of research which should be carefully evaluated in the years to come.

  • Environmental toxicants and cell polarity in the Testis.
    Reproductive toxicology (Elmsford N.Y.), 2018
    Co-Authors: Baiping Mao, Ming Yan, Qingquan Lian, C. Yan Cheng
    Abstract:

    Abstract During spermatogenesis, head-tail cell polarity, apico-basal cell polarity and planar cell polarity (PCP) are remarkably noted in the seminiferous epithelium in which the heads of developing haploid spermatids are pointed to the basement membrane, and with their tails to the tubule lumen. Furthermore, these polarized spermatids are laid unidirectionally across the plane of the seminiferous epithelium, mimicking PCP noted in hair cells of the inner ear. Treatment of rodents with environmental toxicants that lead to germ cell exfoliation, however, are associated with notable changes in spermatid polarity, and defects in spermatid polarity always precede spermatid loss from the epithelium. Studies have also shown that environmental toxicant-induced Sertoli cell or Testis Injury is mediated through changes in actin and/or microtubule (MT) cytoskeletons. Emerging evidence has illustrated that cell polarity and PCP also exert their regulatory effects through changes in cytoskeletal organization. Herein, we discuss and critically evaluate these recent findings, hoping that better efforts can be coordinated by investigators to address this rapidly developing field regarding the role of cell polarity and PCP proteins in toxicant-induced male reproductive dysfunction.

  • Is toxicant-induced Sertoli cell Injury in vitro a useful model to study molecular mechanisms in spermatogenesis?
    Seminars in cell & developmental biology, 2016
    Co-Authors: Dolores D. Mruk, Will M. Lee, Chris K.c. Wong, C. Yan Cheng
    Abstract:

    Sertoli cells isolated from rodents or humans and cultured in vitro are known to establish a functional tight junction (TJ)-permeability barrier that mimics the blood-Testis barrier (BTB) in vivo. This model has been widely used by investigators to study the biology of the TJ and the BTB. Studies have shown that environmental toxicants (e.g., perfluorooctanesulfonate (PFOS), bisphenol A (BPA) and cadmium) that exert their disruptive effects to induce Sertoli cell Injury using this in vitro model are reproducible in studies in vivo. Thus, this in vitro system provides a convenient approach to probe the molecular mechanism(s) underlying toxicant-induced Testis Injury but also to provide new insights in understanding spermatogenesis, such as the biology of cell adhesion, BTB restructuring that supports preleptotene spermatocyte transport, and others. Herein, we provide a brief and critical review based on studies using this in vitro model of Sertoli cell cultures using primary cells isolated from rodent testes vs. humans to monitor environmental toxicant-mediated Sertoli cell Injury. In short, recent findings have shown that environmental toxicants exert their effects on Sertoli cells to induce Testis Injury through their action on Sertoli cell actin- and/or microtubule-based cytoskeleton. These effects are mediated via their disruptive effects on actin- and/or microtubule-binding proteins. Sertoli cells also utilize differential spatiotemporal expression of these actin binding proteins to confer plasticity to the BTB to regulate germ cell transport across the BTB.

  • CADMIUM-INDUCED TESTICULAR Injury
    Toxicology and applied pharmacology, 2009
    Co-Authors: Erica Rosanna Siu, Dolores D. Mruk, Catarina S. Porto, C. Yan Cheng
    Abstract:

    Cadmium (Cd) is an environmental toxicant and an endocrine disruptor in humans and rodents. Several organs (e.g., kidney, liver) are affected by Cd and recent studies have illustrated that the Testis is exceedingly sensitive to Cd toxicity. More important, Cd and other toxicants, such as heavy metals (e.g., lead, mercury) and estrogenic-based compounds (e.g., bisphenols) may account for the recent declining fertility in men among developed countries by reducing sperm count and Testis function. In this review, we critically discuss recent data in the field that have demonstrated the Cd-induced toxicity to the Testis is probably the result of interactions of a complex network of causes. This is likely to involve the disruption of the blood-Testis barrier (BTB) via specific signal transduction pathways and signaling molecules, such as p38 mitogen-activated protein kinase (MAPK). We also summarize current studies on factors that confer and/or regulate the Testis sensitivity to Cd, such as Cd transporters and metallothioneins, the impact of Cd on the Testis as an endocrine disruptor and oxidative stress inducer, and how it may disrupt the Zn(2+) and/or Ca(2+) mediated cellular events. While much work is needed before a unified mechanistic pathway of Cd-induced testicular toxicity emerges, recent studies have helped to identify some of the likely mechanisms and/or events that take place during Cd-induced Testis Injury. Furthermore, some of the recent studies have shed lights on potential therapeutic or preventive approaches that can be developed in future studies by blocking or minimizing the destructive effects of Cd to testicular function in men.

Qi Zhang - One of the best experts on this subject based on the ideXlab platform.

  • aucubin a natural iridoid glucoside attenuates oxidative stress induced Testis Injury by inhibiting jnk and chop activation via nrf2 up regulation
    Phytomedicine, 2019
    Co-Authors: Jie Zhang, Mingya Zhang, Zhiming Zhu, Xiaowen Bao, Chaoxing Ren, Qi Zhang
    Abstract:

    Background Eucommia ulmoides has been used for many years as a successful strategy to treat male infertility. Aucubin (AU) is the active ingredient extracted from Eucommia ulmoides. However, its protective action and exact mechanism on testicular Injury is not yet known. Purpose Here, the protective effect and the mechanism of action of AU on Testis damage under oxidative stress was investigated in vivo and in vitro. Methods As regard the in vivo experiment, male mice were divided into five groups and testicular Injury model was established by Triptolide (TP) (120 μg/kg) intraperitoneal injection for two weeks. Animals in the treatment group were pretreated with an intraperitoneal injection of AU at different doses (5, 10 and 20 mg/kg) for 1 h and subsequently treated with TP (120 μg/kg). At the end of the experimental period, the Testis was collected for biochemical and histological examination. As regard the in vitro experiment, Sertoli cells (SCs) were used to investigate the protective effect and mechanism of action of AU against disruption of the blood-Testis-barrier (BTB) and apoptosis induced by TP via apoptosis detection, western blot, immunofluorescence analysis, and siRNA transient transfection. Results TP-treated animals showed testicular atrophy, BTB disruption, increased ROS levels and spermatogenic dysfunction. Pre-administration of AU resulted in a significant protection on keeping a normal testicular weight, sperm morphology, BTB integrity, and a normal level of oxidative stress markers and antioxidants. Furthermore, AU prevented apoptosis through an effective inhibition of PERK/CHOP and JNK dependent apoptosis pathway, as well as protected the integrity of BTB by up-regulating the expression of tight junction proteins (ZO-1, Occludin, Claudin-11) and gap junction protein (Cx43). The mechanistic study revealed that AU significantly triggered Nrf2 translocation, thus increasing nuclear Nrf2 accumulation and then induced antioxidant enzymes expression in the Testis and SCs. Furthermore, Nrf2 silencing unsuccessfully reversed the increased CHOP and p-JNK expression induced by TP, abolishing the protective effect of AU. Conclusion These results indicate that AU might be considered as a potential protective agent against testicular Injury.

  • mitoq ameliorates Testis Injury from oxidative attack by repairing mitochondria and promoting the keap1 nrf2 pathway
    Toxicology and Applied Pharmacology, 2019
    Co-Authors: Jie Zhang, Mingya Zhang, Lvqi Zhou, Qiaohui Chen, Qi Zhang
    Abstract:

    Abstract Mitochondrial dysfunctions induced by oxidative stress could play a pivotal role in the development of testicular damage and degeneration, leading to impaired fertility in adulthood. MitoQ as mitochondria-targeted antioxidant has been used in many diseases for a long time, but its therapeutic effects on testicular Injury ‘have not been reported yet. Here, we examined the protective action mechanism of MitoQ on testicular Injury from oxidative stress induced by triptolide (TP). Mice were orally administrated with MitoQ (1.3, 2.6 and 5 .2mg/kg, respectively) in a TP-induced model of testicular damage for 14 days. And then Testis injuries were comprehensively evaluated in terms of morphological changes, spermatogenesis assessment, blood-Testis barrier (BTB) integrity, and apoptosis. The results demonstrated MitoQ effectively increased testicular weight, maintained the integrity of BTB, protected microstructure of testicular tissue and sperm morphology by inhibition of oxidative stress. Further mechanism studies revealed that MitoQ markedly activates the Keap1-Nrf2 antioxidative defense system characterized by increasing the expression of Nrf2 and its target genes HO-1 and NQO1. Meanwhile, MitoQ upregulated the expression of mitochondrial dynamics proteins Mfn2 and Drp-1and exerted a protective effect on mitochondria. On this basis, the results from pharmacokinetic study indicated that the MitoQ could enter into Testis tissues after oral administration in despite of the low absolute bioavailability, which provided the material basis for MitoQ in the treatment of testicular damage. More importantly, MitoQ reached mitochondria quickly and had an outstanding feature of mitochondria targeting in Sertoli cells. Therefore, these results provide information for the application of MitoQ against testicular Injury diseases.

  • luteolin ameliorates Testis Injury and blood Testis barrier disruption through the nrf2 signaling pathway and by upregulating cx43
    Molecular Nutrition & Food Research, 2019
    Co-Authors: Jie Zhang, Zhiming Zhu, Ang Zhao, Yanfen Zhou, Hanjie Ying, Qi Zhang
    Abstract:

    SCOPE Luteolin, a natural flavonoid, displays protective activities to testicular tissue. However, the molecular mechanisms are still unclear. In this study, the aim is to identify the protective effects and underlying mechanisms of luteolin against triptolide (TP)-induced damage of testicular tissue. METHODS AND RESULTS Pre-incubation of Sertoli cells (SCs) with luteolin results in a significant reduction of TP-induced apoptotic cells, which occurs concomitantly with the effective inhibition of reactive oxygen species accumulation. Luteolin results in a significant reduction in testicular damage and spermatogenesis dysfunction in a mouse model of testicular damage. Mechanistic studies reveal that luteolin significantly triggers Nrf2 translocation, increases antioxidant response element-luciferase reporter activity, and induces antioxidant enzyme expression. Nrf2 siRNA reduces luteolin-induced protection in SCs. Besides inhibiting apoptosis, luteolin recovers the blood-Testis barrier (BTB) integrity by upregulating connexin43 (Cx43) expression. Moreover, specifically blocked Cx43 activity completely blocks repairmen of luteolin to BTB values. In accordance with in vitro results, luteolin suppresses testicular Injury and spermatogenesis dysfunction by activation of Nrf2 and Cx43 in a testicular Injury model. CONCLUSION Luteolin is identified as a novel active ingredient that contributes to the protective activity in testicular damage through activating the Nrf2 signaling pathway and by upregulating Cx43.

  • Luteolin Ameliorates Testis Injury and Blood–Testis Barrier Disruption through the Nrf2 Signaling Pathway and by Upregulating Cx43
    Molecular nutrition & food research, 2019
    Co-Authors: Jie Zhang, Zhiming Zhu, Ang Zhao, Yanfen Zhou, Hanjie Ying, Qi Zhang
    Abstract:

    SCOPE Luteolin, a natural flavonoid, displays protective activities to testicular tissue. However, the molecular mechanisms are still unclear. In this study, the aim is to identify the protective effects and underlying mechanisms of luteolin against triptolide (TP)-induced damage of testicular tissue. METHODS AND RESULTS Pre-incubation of Sertoli cells (SCs) with luteolin results in a significant reduction of TP-induced apoptotic cells, which occurs concomitantly with the effective inhibition of reactive oxygen species accumulation. Luteolin results in a significant reduction in testicular damage and spermatogenesis dysfunction in a mouse model of testicular damage. Mechanistic studies reveal that luteolin significantly triggers Nrf2 translocation, increases antioxidant response element-luciferase reporter activity, and induces antioxidant enzyme expression. Nrf2 siRNA reduces luteolin-induced protection in SCs. Besides inhibiting apoptosis, luteolin recovers the blood-Testis barrier (BTB) integrity by upregulating connexin43 (Cx43) expression. Moreover, specifically blocked Cx43 activity completely blocks repairmen of luteolin to BTB values. In accordance with in vitro results, luteolin suppresses testicular Injury and spermatogenesis dysfunction by activation of Nrf2 and Cx43 in a testicular Injury model. CONCLUSION Luteolin is identified as a novel active ingredient that contributes to the protective activity in testicular damage through activating the Nrf2 signaling pathway and by upregulating Cx43.

Jie Zhang - One of the best experts on this subject based on the ideXlab platform.

  • Maternal exposure to Di-(2-ethylhexyl) phthalate (DEHP) activates the PI3K/Akt/mTOR signaling pathway in F1 and F2 generation adult mouse Testis.
    Experimental cell research, 2020
    Co-Authors: Jie Zhang, Yuanyuan Yao, Junlin Pan, Xiuxiu Guo, Xiaoying Han, Jun Zhou, Xiao-qian Meng
    Abstract:

    Di-(2-ethylhexyl) phthalate (diethylhexyl phthalate, DEHP) can cause male reproductive damage in rodents and human. Moreover, DEHP is known to promote transgenerational inheritance of adult-onset disease in subsequent generations after maternal exposure during fetal gonadal development. The PI3K/Akt/mTOR signaling pathway has been implicated in germ cell survival following testicular damage. In this study, a F0 gestation DEHP exposure and transgenerational inheritance Testis Injury model was established to study the Testis Injury phenotype and the expression and activation of members of PI3K/Akt/mTOR signaling pathway in the Testis of F1-F3 generation mice. We found that the bodyweight and the anogenital distance (AGD) are reduced only in F1 mice, the sperm motility and deformity decreased in F1-F3 mice, and the testicular histomorphology damagedin F1-F3 mice; however the sperm motility and deformity rates are increased and the histomorphological Injury is repaired during the transgenerational process. We also found the activation of PI3K/Akt/mTOR signaling pathway is enhanced in F1 and F2, and the number of apoptotic cells is decreased in F3 generation mice compared to the control group. These results suggest that the PI3K/Akt/mTOR signaling pathway may be activated to promote the proliferation and differentiation and protect testicular cells from apoptosis in the F1 and F2 generation mice after direct exposure to DEHP.

  • aucubin a natural iridoid glucoside attenuates oxidative stress induced Testis Injury by inhibiting jnk and chop activation via nrf2 up regulation
    Phytomedicine, 2019
    Co-Authors: Jie Zhang, Mingya Zhang, Zhiming Zhu, Xiaowen Bao, Chaoxing Ren, Qi Zhang
    Abstract:

    Background Eucommia ulmoides has been used for many years as a successful strategy to treat male infertility. Aucubin (AU) is the active ingredient extracted from Eucommia ulmoides. However, its protective action and exact mechanism on testicular Injury is not yet known. Purpose Here, the protective effect and the mechanism of action of AU on Testis damage under oxidative stress was investigated in vivo and in vitro. Methods As regard the in vivo experiment, male mice were divided into five groups and testicular Injury model was established by Triptolide (TP) (120 μg/kg) intraperitoneal injection for two weeks. Animals in the treatment group were pretreated with an intraperitoneal injection of AU at different doses (5, 10 and 20 mg/kg) for 1 h and subsequently treated with TP (120 μg/kg). At the end of the experimental period, the Testis was collected for biochemical and histological examination. As regard the in vitro experiment, Sertoli cells (SCs) were used to investigate the protective effect and mechanism of action of AU against disruption of the blood-Testis-barrier (BTB) and apoptosis induced by TP via apoptosis detection, western blot, immunofluorescence analysis, and siRNA transient transfection. Results TP-treated animals showed testicular atrophy, BTB disruption, increased ROS levels and spermatogenic dysfunction. Pre-administration of AU resulted in a significant protection on keeping a normal testicular weight, sperm morphology, BTB integrity, and a normal level of oxidative stress markers and antioxidants. Furthermore, AU prevented apoptosis through an effective inhibition of PERK/CHOP and JNK dependent apoptosis pathway, as well as protected the integrity of BTB by up-regulating the expression of tight junction proteins (ZO-1, Occludin, Claudin-11) and gap junction protein (Cx43). The mechanistic study revealed that AU significantly triggered Nrf2 translocation, thus increasing nuclear Nrf2 accumulation and then induced antioxidant enzymes expression in the Testis and SCs. Furthermore, Nrf2 silencing unsuccessfully reversed the increased CHOP and p-JNK expression induced by TP, abolishing the protective effect of AU. Conclusion These results indicate that AU might be considered as a potential protective agent against testicular Injury.

  • mitoq ameliorates Testis Injury from oxidative attack by repairing mitochondria and promoting the keap1 nrf2 pathway
    Toxicology and Applied Pharmacology, 2019
    Co-Authors: Jie Zhang, Mingya Zhang, Lvqi Zhou, Qiaohui Chen, Qi Zhang
    Abstract:

    Abstract Mitochondrial dysfunctions induced by oxidative stress could play a pivotal role in the development of testicular damage and degeneration, leading to impaired fertility in adulthood. MitoQ as mitochondria-targeted antioxidant has been used in many diseases for a long time, but its therapeutic effects on testicular Injury ‘have not been reported yet. Here, we examined the protective action mechanism of MitoQ on testicular Injury from oxidative stress induced by triptolide (TP). Mice were orally administrated with MitoQ (1.3, 2.6 and 5 .2mg/kg, respectively) in a TP-induced model of testicular damage for 14 days. And then Testis injuries were comprehensively evaluated in terms of morphological changes, spermatogenesis assessment, blood-Testis barrier (BTB) integrity, and apoptosis. The results demonstrated MitoQ effectively increased testicular weight, maintained the integrity of BTB, protected microstructure of testicular tissue and sperm morphology by inhibition of oxidative stress. Further mechanism studies revealed that MitoQ markedly activates the Keap1-Nrf2 antioxidative defense system characterized by increasing the expression of Nrf2 and its target genes HO-1 and NQO1. Meanwhile, MitoQ upregulated the expression of mitochondrial dynamics proteins Mfn2 and Drp-1and exerted a protective effect on mitochondria. On this basis, the results from pharmacokinetic study indicated that the MitoQ could enter into Testis tissues after oral administration in despite of the low absolute bioavailability, which provided the material basis for MitoQ in the treatment of testicular damage. More importantly, MitoQ reached mitochondria quickly and had an outstanding feature of mitochondria targeting in Sertoli cells. Therefore, these results provide information for the application of MitoQ against testicular Injury diseases.

  • luteolin ameliorates Testis Injury and blood Testis barrier disruption through the nrf2 signaling pathway and by upregulating cx43
    Molecular Nutrition & Food Research, 2019
    Co-Authors: Jie Zhang, Zhiming Zhu, Ang Zhao, Yanfen Zhou, Hanjie Ying, Qi Zhang
    Abstract:

    SCOPE Luteolin, a natural flavonoid, displays protective activities to testicular tissue. However, the molecular mechanisms are still unclear. In this study, the aim is to identify the protective effects and underlying mechanisms of luteolin against triptolide (TP)-induced damage of testicular tissue. METHODS AND RESULTS Pre-incubation of Sertoli cells (SCs) with luteolin results in a significant reduction of TP-induced apoptotic cells, which occurs concomitantly with the effective inhibition of reactive oxygen species accumulation. Luteolin results in a significant reduction in testicular damage and spermatogenesis dysfunction in a mouse model of testicular damage. Mechanistic studies reveal that luteolin significantly triggers Nrf2 translocation, increases antioxidant response element-luciferase reporter activity, and induces antioxidant enzyme expression. Nrf2 siRNA reduces luteolin-induced protection in SCs. Besides inhibiting apoptosis, luteolin recovers the blood-Testis barrier (BTB) integrity by upregulating connexin43 (Cx43) expression. Moreover, specifically blocked Cx43 activity completely blocks repairmen of luteolin to BTB values. In accordance with in vitro results, luteolin suppresses testicular Injury and spermatogenesis dysfunction by activation of Nrf2 and Cx43 in a testicular Injury model. CONCLUSION Luteolin is identified as a novel active ingredient that contributes to the protective activity in testicular damage through activating the Nrf2 signaling pathway and by upregulating Cx43.

  • Luteolin Ameliorates Testis Injury and Blood–Testis Barrier Disruption through the Nrf2 Signaling Pathway and by Upregulating Cx43
    Molecular nutrition & food research, 2019
    Co-Authors: Jie Zhang, Zhiming Zhu, Ang Zhao, Yanfen Zhou, Hanjie Ying, Qi Zhang
    Abstract:

    SCOPE Luteolin, a natural flavonoid, displays protective activities to testicular tissue. However, the molecular mechanisms are still unclear. In this study, the aim is to identify the protective effects and underlying mechanisms of luteolin against triptolide (TP)-induced damage of testicular tissue. METHODS AND RESULTS Pre-incubation of Sertoli cells (SCs) with luteolin results in a significant reduction of TP-induced apoptotic cells, which occurs concomitantly with the effective inhibition of reactive oxygen species accumulation. Luteolin results in a significant reduction in testicular damage and spermatogenesis dysfunction in a mouse model of testicular damage. Mechanistic studies reveal that luteolin significantly triggers Nrf2 translocation, increases antioxidant response element-luciferase reporter activity, and induces antioxidant enzyme expression. Nrf2 siRNA reduces luteolin-induced protection in SCs. Besides inhibiting apoptosis, luteolin recovers the blood-Testis barrier (BTB) integrity by upregulating connexin43 (Cx43) expression. Moreover, specifically blocked Cx43 activity completely blocks repairmen of luteolin to BTB values. In accordance with in vitro results, luteolin suppresses testicular Injury and spermatogenesis dysfunction by activation of Nrf2 and Cx43 in a testicular Injury model. CONCLUSION Luteolin is identified as a novel active ingredient that contributes to the protective activity in testicular damage through activating the Nrf2 signaling pathway and by upregulating Cx43.

Nacim Zouari - One of the best experts on this subject based on the ideXlab platform.

  • nicotine induced oxidative stress Testis Injury ache inhibition and brain damage alleviated by mentha spicata
    Inflammopharmacology, 2020
    Co-Authors: Anouar Ben Saad, Ilhem Rjeibi, Noura Brahmi, Elimame Elaloui, Nacim Zouari
    Abstract:

    Nicotine mediates some of the injurious effects caused by consuming tobacco products. The aim of this work is to investigate the protective effects of Mentha spicata extract (ME) supplementation on the Testis and brain of nicotine-induced oxidative damage rats. ME extract showed interesting hydrogen peroxide-scavenging activity. HPLC–DAD analysis of ME revealed the presence of nine compounds among them gallic acid was the major one (165.44 µg/g ME). Thirty-two rats were randomly divided into four groups: control, a nicotine-treated group (1 mg/kg i.p.), a group receiving ME (100 mg/kg), and a group receiving both ME (100 mg/kg) and nicotine (1 mg/kg). After 2 months of treatment, the in vivo results showed that nicotine exhibited an increase in the body, brain, Testis and accessory sex organ weights, sperm count and sperm motility. In addition, exposure to nicotine significantly (p < 0.01) increased acetylcholinesterase level (AChE) in brain, lipid peroxidation level in brain and Testis as compared to control group. The antioxidant enzymes results showed that nicotine treatment induced a significant decrease (p < 0.01) in brain and Testis antioxidant enzymes such as catalase, superoxide dismutase and glutathione peroxidase as compared to control group. Interestingly, pretreatment with ME significantly (p < 0.01) restored the majority of these biological parameters to normal levels, as well as a histological improvement. Obtained results suggest that ME contains promising substances that counteract the nicotine-intoxication and can be efficient in the prevention of brain and Testis toxicity complications.

  • Nicotine-induced oxidative stress, Testis Injury, AChE inhibition and brain damage alleviated by Mentha spicata
    Inflammopharmacology, 2019
    Co-Authors: Anouar Ben Saad, Ilhem Rjeibi, Noura Brahmi, Elimame Elaloui, Nacim Zouari
    Abstract:

    Nicotine mediates some of the injurious effects caused by consuming tobacco products. The aim of this work is to investigate the protective effects of Mentha spicata extract (ME) supplementation on the Testis and brain of nicotine-induced oxidative damage rats. ME extract showed interesting hydrogen peroxide-scavenging activity. HPLC–DAD analysis of ME revealed the presence of nine compounds among them gallic acid was the major one (165.44 µg/g ME). Thirty-two rats were randomly divided into four groups: control, a nicotine-treated group (1 mg/kg i.p.), a group receiving ME (100 mg/kg), and a group receiving both ME (100 mg/kg) and nicotine (1 mg/kg). After 2 months of treatment, the in vivo results showed that nicotine exhibited an increase in the body, brain, Testis and accessory sex organ weights, sperm count and sperm motility. In addition, exposure to nicotine significantly ( p 

Judith C. Hagedorn - One of the best experts on this subject based on the ideXlab platform.

  • Male genital trauma at a level 1 trauma center.
    World journal of urology, 2020
    Co-Authors: Connor S. Mccormick, Mitchell Dumais, Niels V. Johnsen, Bryan B. Voelzke, Judith C. Hagedorn
    Abstract:

    To describe our experience with men admitted to a tertiary care hospital with genital Injury. Adult men with injuries of the genitals, admitted to our institution between January 2013 and June 2018, were identified from our institutional trauma registry. Patient charts were queried to extract mechanism, management, follow-up, and complications. 118 men met inclusion criteria. 39% and 61% sustained penetrating and blunt injuries, respectively. The most common mechanisms of penetrating trauma were external violence (48%) and self-inflicted Injury (40%). The most common mechanisms of blunt trauma were motorcycle crash (33%) and sexual Injury/intercourse (22%). 38% presented with penile and 71% with scrotal injuries. 48% of men with scrotal injuries had concomitant Testis Injury. 9.3% presented with both a penile and a scrotal Injury. Concomitant urethral injuries were found in 17% of all genital injuries. Genital trauma was more common in the summer months. 74% of all genital injuries were managed operatively, with surgery more common after penetrating Injury (89% vs 64%, p value 

  • Male genital trauma at a level 1 trauma center
    World Journal of Urology, 2020
    Co-Authors: Connor S. Mccormick, Mitchell Dumais, Niels V. Johnsen, Bryan B. Voelzke, Judith C. Hagedorn
    Abstract:

    Objectives To describe our experience with men admitted to a tertiary care hospital with genital Injury. Methods Adult men with injuries of the genitals, admitted to our institution between January 2013 and June 2018, were identified from our institutional trauma registry. Patient charts were queried to extract mechanism, management, follow-up, and complications. Results 118 men met inclusion criteria. 39% and 61% sustained penetrating and blunt injuries, respectively. The most common mechanisms of penetrating trauma were external violence (48%) and self-inflicted Injury (40%). The most common mechanisms of blunt trauma were motorcycle crash (33%) and sexual Injury/intercourse (22%). 38% presented with penile and 71% with scrotal injuries. 48% of men with scrotal injuries had concomitant Testis Injury. 9.3% presented with both a penile and a scrotal Injury. Concomitant urethral injuries were found in 17% of all genital injuries. Genital trauma was more common in the summer months. 74% of all genital injuries were managed operatively, with surgery more common after penetrating Injury (89% vs 64%, p value