scholarly journals Lycopene supplementation prevents reactive oxygen species mediated apoptosis in Sertoli cells of adult albino rats exposed to polychlorinated biphenyls

2013 ◽  
Vol 6 (2) ◽  
pp. 83-92 ◽  
Author(s):  
Gunasekaran Krishnamoorthy ◽  
Kandaswamy Selvakumar ◽  
Prabhu Venkataraman ◽  
Perumal Elumalai ◽  
Jagadeesan Arunakaran
Keyword(s):  
Oxidative Stress ◽  
Polychlorinated Biphenyls ◽  
Sertoli Cell ◽  
Sertoli Cells ◽  
Caspase 3 ◽  
Sperm Count ◽  
Reactive Oxygen ◽  
The Other ◽  
Sperm Production ◽  
Other Hand

Abstract Sertoli cell proliferation is attenuated before attaining puberty and the number is fixed in adult testes. Sertoli cells determine both testis size and daily sperm production by providing physical and metabolic support to spermatogenic cells. Polychlorinated biphenyls (PCBs) exposure disrupts functions of Sertoli cells causing infertility with decreased sperm count. On the other hand, lycopene is improving sperm count and motility by reducing oxidative stress in humans and animals. Hence we hypothesized that PCBs-induced infertility might be due to Sertoli cell apoptosis mediated by oxidative stress and lycopene might prevent PCBs-induced apoptosis by acting against oxidative stress. To test this hypothesis, animals were treated with vehicle control, lycopene, PCBs and PCBs + lycopene for 30 days. After the experimental period, the testes and cauda epididymidis were removed for isolation of Sertoli cells and sperm, respectively. We observed increased levels of oxidative stress markers (H2O2 and LPO) levels, increased expression of apoptotic molecules (caspase-8, Bad, Bid, Bax, cytochrome C and caspase-3), decreased anti-apoptotic (Bcl2) molecule and elevated apoptotic marker activity (caspase-3) in Sertoli cells of PCBs-exposed animals. These results were associated with decreased sperm count and motility in PCBs exposed animals. On the other hand, lycopene prevented the elevation of Sertoli cellular apoptotic parameters and prevented the reduction of sperm parameters (count and motility). The data confirmed that lycopene as an antioxidant scavenged reactive oxygen substances, prevented apoptosis, maintained normal function in Sertoli cells and helped to provide physical and metabolic support for sperm production, thereby treating infertility in men.

Nobiletin ameliorates nonylphenol-induced testicular damage by improving biochemical, steroidogenic, hormonal, spermatogenic, apoptotic and histological profile

2020 ◽  
pp. 096032712095000
Author(s):  
Muhammad Umar Ijaz ◽  
Arfa Tahir ◽  
Abdul Samad ◽  
Haseeb Anwar
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Sperm Count ◽  
Thiobarbituric Acid ◽  
Male Rats ◽  
Plasma Testosterone ◽  
Sperm Production ◽  
Thiobarbituric Acid Reactive Substances ◽  
Apoptotic Protein ◽  
Daily Sperm Production

Nonylphenol (NP) is an environmental contaminant, which adversely affects the male fertility due to endocrine disruption and generation of oxidative stress. The current research was planned to assess the effects of nobiletin (NOB), a polymethoxyflavone, on NP-induced testicular damages. Twenty-four male rats were divided into 4 groups: control (0.1% DMSO), NP group (50 mg/kg), NP+NOB group (50 mg/kg + 25 mg/kg), and NOB group (25 mg/kg). Our results revealed that NP brought down the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GSR), while elevated the level of thiobarbituric acid reactive substances (TBARS). Additionally, NP decreased the level of follicle-stimulating hormone (FSH), luteinizing hormone (LH), plasma testosterone, daily sperm production (DSP), epididymal sperm count, viability, motility, gene expression of testicular steroidogenic enzymes (StAR, 3β-HSD and 17β-HSD) and anti-apoptotic protein (Bcl-2), as well as number of spermatogenic cells belonging to various stages. Whereas, sperm (head, mid-piece/neck and tail) abnormalities, expression of apoptotic proteins (Bax and caspase-3), and histopathological damages were increased. However, NOB remarkably reversed all the damages caused by NP. Therefore, it is deduced that NOB could be used as a potential therapeutic to counter the NP-prompted oxidative stress and apoptotic damages in testes.

SERUM GONADOTROPHINS, TESTOSTERONE AND SPERMATOGENESIS IN SUBFERTILE MEN

1977 ◽  
Vol 86 (3) ◽  
pp. 651-658 ◽  
Author(s):  
J. H. Aafjes ◽  
J. C. M. van der Vijver ◽  
R. Docter ◽  
P. E. Schenck
Keyword(s):  
Partial Correlation ◽  
Sperm Count ◽  
Correlation Coefficients ◽  
Serum Levels ◽  
Significant Negative Correlation ◽  
The Other ◽  
Sperm Production ◽  
Positive Correlation ◽  
Natural Logarithm ◽  
Biopsy Score

ABSTRACT In 210 subfertile men there existed a significant positive correlation between serum FSH and LH (0.41). No correlation was observed between the gonadotrophin levels and testosterone. In contrast to this FSH as well as LH were negatively correlated with the natural logarithm (In) of the sperm count/ml ejaculate (−0.44 and −0.18, respectively). When the positive correlation which existed between FSH and LH was used to calculate partial correlation coefficients, the coefficient between FSH and ln sperm count did hardly change (−0.41) the coefficient between LH and ln sperm count on the other hand became insignificant (−0.05). This suggests that spermatogenesis influences FSH serum levels in subfertile men by a decreased suppression when sperm production is diminished. Testicular biopsies taken from 97 of these patients were used to determine biopsy scores. These scores showed a significant negative correlation with FSH (−0.34) and a positive one with ln sperm count/ml ejaculate (0.45). Interestingly the biopsy score of 16 patients who fertilized their wives, was found to be higher compared with the score of the other patients who did not fertilize. The number of sperm/ml ejaculate and the FSH values of these 2 groups of biopsied patients were, however, not significantly different. This leads to the conclusion that the biopsy score is a better parameter for the evaluation of oligospermic men than either sperm count or FSH serum values.

Modification of spermatozoa quality in mature small ruminants

2012 ◽  
Vol 24 (1) ◽  
pp. 13 ◽  
Author(s):  
G. B. Martin ◽  
T. Jorre de St Jorre ◽  
F. A. Al Mohsen ◽  
I. A. Malecki
Keyword(s):  
Large Body ◽  
Small Ruminants ◽  
Cell Loss ◽  
Testicular Tissue ◽  
The Other ◽  
Sperm Production ◽  
Testicular Mass ◽  
Other Hand ◽  
Sperm Survival ◽  
Sperm Output

This review is based largely, but not entirely, on the assumption that gamete quality is directly linked to sperm output and thus testicular mass, an approach made necessary by the absence of a large body of data on factors that affect gamete quality in ruminants. On the other hand, there is a change in the efficiency of sperm production per gram of testicular tissue when the testis is growing or shrinking, a clear indicator of changes in the rates of cell loss during the process of spermatogenesis, probably through apoptosis. We therefore postulate that the spermatozoa that do survive when the testis is shrinking are of a lower quality than those that are produced when the testis is growing and the rate of sperm survival is increasing. In adult small ruminants in particular, testicular mass and sperm production are highly labile and can be manipulated by management of photoperiod (melatonin), nutrition, genetics and behaviour (‘mating pressure’). Importantly, these factors do not act independently of each other – rather, the outcomes in terms of sperm production are dictated by interactions. It therefore seems likely that spermatozoa quality will be affected by these same factors, but definitive answers await detailed studies.

Effects of infliximab against carbon tetrachloride-induced intestinal injury via lipid peroxidation and apoptosis

2019 ◽  
Vol 38 (11) ◽  
pp. 1275-1282
Author(s):  
A Pergel ◽  
L Tümkaya ◽  
MK Çolakoğlu ◽  
G Demiral ◽  
S Kalcan ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Caspase 3 ◽  
Inhalation Exposure ◽  
Isotonic Saline ◽  
Neutrophil Infiltration ◽  
Intestinal Injury ◽  
The Other ◽  
Control Group ◽  
Sprague Dawley ◽  
Other Hand

Carbon tetrachloride (CCL4) is often employed in the production of chlorofluorocarbons, petroleum refining, oil and rubber processing, and laboratory applications. Oral, subcutaneous, and inhalation exposure to CCL4 in animal studies have been shown to be capable of leading to various types of cancer (benign and malignant, liver, breast, and adrenal gland tumors). The present study also evaluated the protective role of infliximab (INF) against the deleterious effects of CCL4 on the intestinal system. Twenty-four male Sprague-Dawley rats were randomly assigned into three groups, control ( n = 8), CCL4 ( n = 8), and CCL4 + INF ( n = 8). The control group received 1 mL isotonic saline solution only via intraperitoneal (i.p.) injection. The CCL4 group received a single i.p. dose of 2 mL/kg CCL4. The CCL4 + INF group received a single i.p. dose of 7 mg/kg INF followed 24 h later by a single dose of 2 mL/kg CCL4. All rats were euthanized 2 days following drug administration. CCL4 group samples also exhibited diffuse loss of enterocytes, vascular congestion, neutrophil infiltration, an extension of the subepithelial space and significant epithelial lifting along the length of the villi with a few denuded villous tips. In addition, CCL4 treatment increased intestinal malondialdehyde (MDA) level and caspase-3 positivity. On the other hand, INF decreased MDA levels, caspase-3 positivity, and loss of villous. Our findings suggest that CCL4 appears to exert a highly deleterious effect on the intestinal mucosa. On the other hand, INF is effective in preventing this CCL4-induced intestinal injury by reducing oxidative stress and apoptosis.

scholarly journals Does the Interdependence between Oxidative Stress and Inflammation Explain the Antioxidant Paradox?

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Subrata Kumar Biswas
Keyword(s):  
Oxidative Stress ◽  
Chronic Diseases ◽  
Inflammatory Process ◽  
The Other ◽  
Present Review ◽  
Low Grade ◽  
Inflammatory Pathways ◽  
Pathological Conditions ◽  
Other Hand ◽  
And Oxidative Stress

Oxidative stress has been implicated in many chronic diseases. However, antioxidant trials are so far largely unsuccessful as a preventive or curative measure. Chronic low-grade inflammatory process, on the other hand, plays a central role in the pathogenesis of a number of chronic diseases. Oxidative stress and inflammation are closely related pathophysiological processes, one of which can be easily induced by another. Thus, both processes are simultaneously found in many pathological conditions. Therefore, the failure of antioxidant trials might result from failure to select appropriate agents that specifically target both inflammation and oxidative stress or failure to use both antioxidants and anti-inflammatory agents simultaneously or use of nonselective agents that block some of the oxidative and/or inflammatory pathways but exaggerate the others. To examine whether the interdependence between oxidative stress and inflammation can explain the antioxidant paradox we discussed in the present review the basic aspects of oxidative stress and inflammation and their relationship and dependence.

scholarly journals Effects of aerobic training on oxidative stress and inflammation in rats exposed to controlled emissions of carbon monoxide (CO) and nitrogen dioxide (NO2)

2020 ◽  
Vol 8 (2) ◽  
pp. 099-110
Author(s):  
Tito S. Albérick I ◽  
Nsompi Florent ◽  
Messan Folly ◽  
Kpatcha Tchazou ◽  
Lawani M. Mansourou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Monoxide ◽  
Nitrogen Dioxide ◽  
Aerobic Exercise ◽  
Ambient Air ◽  
Repeated Exposure ◽  
The Other ◽  
Training Block ◽  
Other Hand ◽  
Tnf Α

The objective of this study is to determine the effects of isolated exercise and those of repeated exercise on oxidative stress and the inflammatory process following exposure to carbon monoxide (CO) and nitrogen dioxide (NO2). Material and Method: 15 male Wistar rats, all eight weeks old, were randomly assigned to three groups. CO and NO2 were produced by the combustion of diesel fuel using a device contained in a sealed metal box and supplied with ambient air by a pump. The ranges of CO and NO2 concentrations to which the rats were exposed ranged from 35 to 45 ppm and 0.2 to 0.3 ppm, respectively. The aerobic workouts were performed on a rat treadmill. Blood samples were taken 24 hours after completion of handling at D4, D9 and D14. Variables studied were Malondialdehyde (MDA) and Tumor Necrosis Factor-alpha (TNF-α). Results: Aerobic endurance training after repeated exposure to CO and NO2 induces at the end of the first training block (D4) a significant increase (p ˂ 0.01) in MDA and TNF-α. On the other hand, the second block (D9) and the third training block (D14) induced a significant decrease (p ˂ 0.01) in these same parameters. Conclusion: Aerobic exercise practiced in isolation exacerbates the oxidative stress and inflammation induced by exposure to CO and NO2. On the other hand, regular aerobic exercise in a less polluted environment, following five days of recovery, significantly reduces the high levels of oxidative stress and inflammation caused by repeated exposure to automobile pollutants.

scholarly journals The Role of Mitochondrial Impairment and Oxidative Stress in the Pathogenesis of Lithium-Induced Reproductive Toxicity in Male Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Mohammad Mehdi Ommati ◽  
Mohammad Reza Arabnezhad ◽  
Omid Farshad ◽  
Akram Jamshidzadeh ◽  
Hossein Niknahad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adverse Effects ◽  
Reproductive Toxicity ◽  
The Other ◽  
Mitochondrial Depolarization ◽  
Mitochondrial Impairment ◽  
Other Hand ◽  
Wide Range ◽  
The Impact ◽  
Testis Tissue

Lithium (Li+) is prescribed against a wide range of neurological disorders. Besides its excellent therapeutic properties, there are several adverse effects associated with Li+. The impact of Li+ on renal function and diabetes insipidus is the most common adverse effect of this drug. On the other hand, infertility and decreased libido is another complication associated with Li+. It has been found that sperm indices of functionality, as well as libido, is significantly reduced in Li+-treated men. These adverse effects might lead to drug incompliance and the cessation of drug therapy. Hence, the main aims of the current study were to illustrate the mechanisms of adverse effects of Li+ on the testis tissue, spermatogenesis process, and hormonal changes in two experimental models. In the in vitro experiments, Leydig cells (LCs) were isolated from healthy mice, cultured, and exposed to increasing concentrations of Li+ (0, 10, 50, and 100 ppm). In the in vivo section of the current study, mice were treated with Li+ (0, 10, 50, and 100 ppm, in drinking water) for five consecutive weeks. Testis and sperm samples were collected and assessed. A significant sign of cytotoxicity (LDH release and MTT assay), along with disrupted testosterone biosynthesis, impaired mitochondrial indices (ATP level and mitochondrial depolarization), and increased biomarkers of oxidative stress were detected in LCs exposed to Li+. On the other hand, a significant increase in serum and testis Li+ levels were detected in drug-treated mice. Moreover, ROS formation, LPO, protein carbonylation, and increased oxidized glutathione (GSSG) were detected in both testis tissue and sperm specimens of Li+-treated mice. Several sperm anomalies were also detected in Li+-treated animals. On the other hand, sperm mitochondrial indices (mitochondrial dehydrogenases activity and ATP levels) were significantly decreased in drug-treated groups where mitochondrial depolarization was increased dose-dependently. Altogether, these data mention oxidative stress and mitochondrial impairment as pivotal mechanisms involved in Li+-induced reproductive toxicity. Therefore, based on our previous publications in this area, therapeutic options, including compounds with high antioxidant properties that target these points might find a clinical value in ameliorating Li+-induced adverse effects on the male reproductive system.

scholarly journals Upregulation of Peroxiredoxin 3 Protects Afg3l2-KO Cortical Neurons In Vitro from Oxidative Stress: A Paradigm for Neuronal Cell Survival under Neurodegenerative Conditions

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Barbara Bettegazzi ◽  
Ilaria Pelizzoni ◽  
Floramarida Salerno Scarzella ◽  
Lisa Michelle Restelli ◽  
Daniele Zacchetti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cortical Neurons ◽  
Mitochondrial Dynamics ◽  
Neuronal Cell ◽  
The Other ◽  
Antioxidant Defenses ◽  
Glutathione Depletion ◽  
Other Hand ◽  
Peroxiredoxin 3

Several neurodegenerative disorders exhibit selective vulnerability, with subsets of neurons more affected than others, possibly because of the high expression of an altered gene or the presence of particular features that make them more susceptible to insults. On the other hand, resilient neurons may display the ability to develop antioxidant defenses, particularly in diseases of mitochondrial origin, where oxidative stress might contribute to the neurodegenerative process. In this work, we investigated the oxidative stress response of embryonic fibroblasts and cortical neurons obtained from Afg3l2-KO mice. AFG3L2 encodes a subunit of a protease complex that is expressed in mitochondria and acts as both quality control and regulatory enzyme affecting respiration and mitochondrial dynamics. When cells were subjected to an acute oxidative stress protocol, the survival of AFG3L2-KO MEFs was not significantly influenced and was comparable to that of WT; however, the basal level of the antioxidant molecule glutathione was higher. Indeed, glutathione depletion strongly affected the viability of KO, but not of WT MEF, thereby indicating that oxidative stress is more elevated in KO MEF even though well controlled by glutathione. On the other hand, when cortical KO neurons were put in culture, they immediately appeared more vulnerable than WT to the acute oxidative stress condition, but after few days in vitro, the situation was reversed with KO neurons being more resistant than WT to acute stress. This compensatory, protective competence was not due to the upregulation of glutathione, rather of two mitochondrial antioxidant proteins: superoxide dismutase 2 and, at an even higher level, peroxiredoxin 3. This body of evidence sheds light on the capability of neurons to activate neuroprotective pathways and points the attention to peroxiredoxin 3, an antioxidant enzyme that might be critical for neuronal survival also in other disorders affecting mitochondria.

scholarly journals Manganese-Induced Nephrotoxicity Is Mediated through Oxidative Stress and Mitochondrial Impairment

2020 ◽  
Vol 4 (2) ◽  
pp. 1-10 ◽  
Author(s):  
Amir Mohammad Niknahad ◽  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Leila Moezi ◽  
Reza Heidari
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Essential Element ◽  
The Other ◽  
Tubular Atrophy ◽  
Mitochondrial Impairment ◽  
Other Hand ◽  
Markers Of Oxidative Stress ◽  
Dehydrogenases Activity

Manganese (Mn) is an essential element that is incorporated in various metabolic pathways and enzyme structures. On the other hand, a range of adverse effects has been described in association with Mn overexposure. Mn is a well-known neurotoxic agent in mammals. Renal injury is another adverse effect associated with Mn intoxication. No precise mechanism for Mn nephrotoxicity has been identified so far. The current study was designed to evaluate the potential mechanisms of Mn-induced renal injury. Rats were treated with Mn (20 and 40 mg/mL, respectively, in drinking water) for 30 consecutive days. Markers of oxidative stress, as well as several mitochondrial indices, were assessed in the kidney tissue. Renal injury was evident in Mn-treated animals, as judged by a significant increase in serum BUN and creatinine. Moreover, urinalysis revealed a significant increase in urine glucose, phosphate, and protein in Mn-treated rats. Kidney histopathological alterations, including tubular atrophy, interstitial inflammation, and necrosis, were also detected in Mn-treated animals. Biomarkers of oxidative stress, including an increment in reactive oxygen species (ROS), lipid peroxidation, and oxidized glutathione (GSSG), were detected in Mn-treated groups. On the other hand, kidney glutathione (GSH) stores and total antioxidant capacity were depleted in Mn groups. Mn exposure was associated with significant mitochondrial depolarization, decreased mitochondrial dehydrogenases activity, mitochondrial permeabilization, and depletion of adenosine tri-phosphate (ATP) content. These data highlight oxidative stress and mitochondrial impairment as potential mechanisms involved in Mn-induced renal injury.

TWO TYPES OF SERTOLI CELLS IN MAN

1969 ◽  
Vol 61 (1) ◽  
pp. 111-116 ◽  
Author(s):  
Svend G. Johnsen
Keyword(s):  
Nucleic Acids ◽  
Sertoli Cell ◽  
Sertoli Cells ◽  
Picric Acid ◽  
Type A ◽  
The Other ◽  
Type B ◽  
Iron Alum ◽  
Haematoxylin Staining

ABSTRACT By means of iron haematoxylin staining carefully differentiated by either picric acid or iron alum, Sertoli cells may be differentiated into two types, one (type A) containing unstained nuclei and the other (type B) intensely stained nuclei. No intermediate forms appear to be present. The two types are most easily found in the Sertoli-cell-only syndrome but they are present in the testes with spermatogenesis although type B is rare. The immature (pro-) Sertoli cells in infantile testes also display the two types. The two types of Sertoli cells differ in their degree of binding between nucleic acids and nucleic protein. The significance of the existence of these two types is discussed.

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