scholarly journals Toxicity Investigation of Nano-SiO2 on Male Reproductive System in Pubertal Mice

2021 ◽  
Author(s):  
Fanli Sun ◽  
Xuying Wang ◽  
Pinzheng Zhang ◽  
Ziyun Chen ◽  
Zhiyi Guo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reproductive System ◽  
Intraperitoneal Injection ◽  
Sperm Quality ◽  
Underlying Mechanism ◽  
Reproductive Organs ◽  
Male Reproductive System ◽  
Reproductive Capacity ◽  
Apoptotic Pathway ◽  
And Function

Abstract BackgroundPuberty is a crucial stage to gain reproductive capacity, but it is also a period vulnerable to exogenous materials. While exposure to nanoparticles (NPs) has been linked to toxic responses in reproductive system in previous findings, little is known about the age-dependent effect of NPs, let alone the underlying mechanism. In the present study, we assessed male fertility parameters and explored its mechanism following intraperitoneal exposure to Nano-Silicon dioxide (Nano-SiO2) in mice during puberty.Methods40 mice aged 5 weeks were divided into 2 groups after 1 week acclimation and then exposed to 40mg/kg Nano-SiO2 dissolved in saline or vehicle controls by intraperitoneal injection every day over a period of 7-day, respectively. Changes in the structure and function of male reproductive organs were detected after exposure.ResultsNano-SiO2 exposed through intraperitoneal injection could cause damage to the testicular and epididymal histological architecture and reduce the level of sex hormone (testosterone), leading to a decrease in sperm quality and quantity. Furthermore, Nano-SiO2 could induce oxidative stress and inflammation in male reproductive tissues, indicated by reduced activity of antioxidants (superoxide dismutase, SOD) and increased level of the lipid peroxidation marker (malondialdehyde, MDA), which leads to the activation of cell apoptosis.ConclusionExposure to Nano-SiO2 in pubertal mice could cause toxicity on male reproductive system via inducing oxidative stress and activating TNF-α mediated apoptotic pathway.

scholarly journals Pyrethroids Toxicity to Male Reproductive System and Offspring as a Function of Oxidative Stress Induction: Rodent Studies

2021 ◽  
Vol 12 ◽  
Author(s):  
Xu Zhang ◽  
Tongtong Zhang ◽  
Xiaohan Ren ◽  
Xinglin Chen ◽  
ShangQian Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Sperm Motility ◽  
Reproductive System ◽  
Sperm Quality ◽  
Sperm Count ◽  
Meta Analysis ◽  
Serum Testosterone ◽  
Male Reproductive System ◽  
Serum Testosterone Level ◽  
Testis Weight

Pyrethroids may be related to male reproductive system damage. However, the results of many previous studies are contradictory and uncertain. Therefore, a systematic review and a meta-analysis were performed to assess the relationship between pyrethroid exposure and male reproductive system damage. A total of 72 articles were identified, among which 57 were selected for meta-analysis, and 15 were selected for qualitative analysis. Pyrethroid exposure affected sperm count (SMD= -2.0424; 95% CI, -2.4699 to -1.6149), sperm motility (SMD=-3.606; 95% CI, -4.5172 to -2.6948), sperm morphology (SMD=2.686; 95% CI, 1.9744 to 3.3976), testis weight (SMD=-1.1591; 95% CI, -1.6145 to -0.7038), epididymal weight (SMD=-1.1576; 95% CI, -1.7455 to -0.5697), and serum testosterone level (SMD=-1.9194; 95% CI, -2.4589 to -1.3798) in the studies of rats. We found that gestational and lactational exposure to pyrethroids can reduce sperm count (SMD=1.8469; 95% CI, -2.9010 to -0.7927), sperm motility (SMD=-2.7151; 95% CI, -3.9574 to -1.4728), testis weight (SMD=-1.4361; 95% CI, -1.8873 to -0.9848), and epididymal weight (SMD=-0.6639; 95% CI, -0.9544 to -0.3733) of F1 offspring. Exposure to pyrethroids can increase malondialdehyde (SMD=3.3451; 95% CI 1.9914 to 4.6988) oxide in testes and can reduce the activities of glutathione (SMD=-2.075; 95% CI -3.0651 to -1.0848), superoxide dismutase (SMD=-2.4856; 95% CI -3.9612 to -1.0100), and catalase (SMD=-2.7564; 95% CI -3.9788 to -1.5340). Pyrethroid exposure and oxidative stress could damage male sperm quality. Gestational and lactational pyrethroid exposure affects the reproductive system of F1 offspring.

scholarly journals Bacterial Infections Affect Male Fertility: A Focus on the Oxidative Stress-Autophagy Axis

2021 ◽  
Vol 9 ◽  
Author(s):  
Sutian Wang ◽  
Kunli Zhang ◽  
Yuchang Yao ◽  
Jianhao Li ◽  
Shoulong Deng
Keyword(s):  
Oxidative Stress ◽  
Reproductive System ◽  
Bacterial Infections ◽  
Reproductive Organs ◽  
Innate Immune ◽  
Male Reproductive System ◽  
Pathogenic Microorganisms ◽  
Immune Functions ◽  
Molecular Patterns ◽  
Multiple Signaling

Numerous factors trigger male infertility, including lifestyle, the environment, health, medical resources and pathogenic microorganism infections. Bacterial infections of the male reproductive system can cause various reproductive diseases. Several male reproductive organs, such as the testicles, have unique immune functions that protect the germ cells from damage. In the reproductive system, immune cells can recognize the pathogen-associated molecular patterns carried by pathogenic microorganisms and activate the host’s innate immune response. Furthermore, bacterial infections can lead to oxidative stress through multiple signaling pathways. Many studies have revealed that oxidative stress serves dual functions: moderate oxidative stress can help clear the invaders and maintain sperm motility, but excessive oxidative stress will induce host damage. Additionally, oxidative stress is always accompanied by autophagy which can also help maintain host homeostasis. Male reproductive system homeostasis disequilibrium can cause inflammation of the genitourinary system, influence spermatogenesis, and even lead to infertility. Here, we focus on the effect of oxidative stress and autophagy on bacterial infection in the male reproductive system, and we also explore the crosslink between oxidative stress and autophagy during this process.

scholarly journals Necroptosis promotes the Aging of the Male Reproductive System in Mice

2017 ◽  
Author(s):  
Dianrong Li ◽  
Lingjun Meng ◽  
Tao Xu ◽  
Yaning Su ◽  
Xiao Liu ◽  
...  
Keyword(s):  
Reproductive System ◽  
Accelerated Aging ◽  
Reproductive Organs ◽  
Male Reproductive System ◽  
Necrotic Cell Death ◽  
Wild Type ◽  
Necrotic Cell ◽  
Age Related ◽  
And Function ◽  
Age Related Changes

AbstractNecroptosis is a form of programmed necrotic cell death in mammals that is mediated by a pair of kinases, RIP1 and RIP3, as well as the RIP3 substrate MLKL. We report here that male reproductive organs of both RIP3-and MLKL-knockout mice retain “youthful” morphology and function into advanced age, while those of age-matched wild type mice deteriorate. The RIP3 phosphorylation of MLKL, the activation marker of necroptosis, is detected in spermatogonial stem cells in the testes of old but not in young wild type mice. When the testes of young wild type mice are given a local necroptotic stimulus, their reproductive organs showed accelerated aging. Feeding of wild type mice with an RIP1 inhibitor prior to the normal onset of age-related changes in their reproductive organs blocked the appearance of signs of aging. Thus, necroptosis in testes promotes the aging-associated deterioration of the male reproductive system in mice.

scholarly journals RIPK1-RIPK3-MLKL-dependent necrosis promotes the aging of mouse male reproductive system

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Dianrong Li ◽  
Lingjun Meng ◽  
Tao Xu ◽  
Yaning Su ◽  
Xiao Liu ◽  
...  
Keyword(s):  
Reproductive System ◽  
Accelerated Aging ◽  
Reproductive Organs ◽  
Male Reproductive System ◽  
Necrotic Cell Death ◽  
Wild Type ◽  
Necrotic Cell ◽  
Age Related ◽  
And Function ◽  
Age Related Changes

A pair of kinases, RIPK1 and RIPK3, as well as the RIPK3 substrate MLKL cause a form of programmed necrotic cell death in mammals termed necroptosis. We report here that male reproductive organs of both Ripk3- and Mlkl-knockout mice retain ‘youthful’ morphology and function into advanced age, while those of age-matched wild-type mice deteriorate. The RIPK3 phosphorylation of MLKL, the activation marker of necroptosis, is detected in spermatogonial stem cells in the testes of old but not in young wild-type mice. When the testes of young wild-type mice are given a local necroptotic stimulus, their reproductive organs showed accelerated aging. Feeding of wild-type mice with an RIPK1 inhibitor prior to the normal onset of age-related changes in their reproductive organs blocked the appearance of signs of aging. Thus, necroptosis in testes promotes the aging-associated deterioration of the male reproductive system in mice.

scholarly journals Epididymis Expresses the Highest 5′-Deiodinase Activity in the Male Reproductive System: Kinetic Characterization, Distribution, and Hormonal Regulation

Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 4209-4217 ◽  
Author(s):  
Brenda Anguiano ◽  
Nuri Aranda ◽  
Guadalupe Delgado ◽  
Carmen Aceves
Keyword(s):  
Reproductive System ◽  
Hormonal Regulation ◽  
Reproductive Tract ◽  
Pcr Amplification ◽  
Male Reproductive System ◽  
Reverse T3 ◽  
Physiological Relevance ◽  
Kinetic Pattern ◽  
And Function ◽  
Menten Constant

We characterized the enzymes that catalyze the deiodination of T4 to T3 in the male reproductive tract. Testis, epididymis (EPI), seminal vesicles, prostate, bulbourethral glands, spermatozoa, and semen were taken from sexually mature rats (300 g). Iodothyronine 5′-deiodinase (5′-D) activity was quantified by the radiolabeled-iodide-release method. 5′-D activity was 10-fold higher in EPI and semen than in the rest of the tissues. In EPI, semen, and prostate, the enzymatic activity was completely inhibited by 1 mm 6-n-propyl-2-thiouracil, whereas in the other tissues the inhibition was partial (50%). The high susceptibility to 6-n-propyl-2-thiouracil inhibition, a ping-pong kinetic pattern, and low cofactor (Michaelis Menten constant for dithiothreitol = 0.7 mm) and high substrate (Michaelis Menten constant for reverse T3 = 0.4 μm) requirements indicate that EPI 5′-D corresponds to type 1 deiodinase (D1). Real-time RT-PCR amplification of D1 mRNA in this tissue confirms this conclusion. The highest EPI D1 expression occurred at the onset of puberty and sexual maturity, and in the adult, this activity was more abundant in corpus and caput than in the caudal region. EPI D1 expression was elevated under conditions of hyperthyroidism and with addition of 17β-estradiol. Our data also showed a direct association between D1 and a functional epididymis marker, the neutral α-glucosidase enzyme, suggesting that local generation of T3 could be associated with the development and function of EPI and/or spermatozoa maturation. Further studies are necessary to analyze the possible physiological relevance of 5′-D in the male reproductive system.

scholarly journals Sperm oxidative stress: clinical significance and management

2021 ◽  
pp. 19-27
Author(s):  
S. I. Gamidov ◽  
T. V. Shatylko ◽  
A. Yu. Popova ◽  
N. G. Gasanov ◽  
R. S. Gamidov
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reproductive System ◽  
Molecular Mechanisms ◽  
Assisted Reproductive Technologies ◽  
Reactive Oxygen ◽  
Reproductive Technologies ◽  
Male Reproductive System ◽  
Antioxidant Systems ◽  
Oxygen Species

Oxidative stress is one of the leading causes of sperm dysfunction. Excessive amounts of reactive oxygen species can damage sperm membranes and disrupt their DNA integrity, which affects not only the likelihood of getting pregnant naturally, but also the clinical outcomes of assisted reproductive technologies and the risk of miscarriage. Sperm cells are extremely vulnerable to oxidative stress, given the limited functional reserve of their antioxidant systems and the DNA repair apparatus. Lifestyle factors, most of which are modifiable, often trigger generation of reactive oxygen species.  Both the lifestyle modification and use of antioxidant dietary supplements are adequate and compatible ways to combat male oxidative stress-associated infertility. The search for other internal and external sources of reactive oxygen species, the identification of the etiology of oxidative stress and treatment of respective diseases are necessary for the successful regulation of redox processes in the male reproductive system in clinical practice, which is required not only to overcome infertility, but also to prevent induced epigenetic disorders in subsequent generations. The article presents the analysis of the molecular mechanisms of male idiopathic infertility. The authors provide an overview of how to prevent oxidative stress as one of the causes of subfebrile fever. The article provides an overview of modern therapeutics, as well as the options for eliminating the consequences of the effect of reactive oxygen species on spermatogenesis and male reproductive system in general.

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