scholarly journals Chitosan/Selenium Nanoparticles Attenuate Diclofenac Sodium-Induced Testicular Toxicity in Male Rats

Crystals ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1477
Author(s):  
Samy M. El-Megharbel ◽  
Fawziah A. Al-Salmi ◽  
Sarah Al-Harthi ◽  
Khadeejah Alsolami ◽  
Reham Z. Hamza
Keyword(s):  
Oxidative Stress ◽  
Diclofenac Sodium ◽  
Chitosan Nanoparticles ◽  
Reproductive Toxicity ◽  
Male Reproduction ◽  
Male Rats ◽  
Antioxidant Enzyme Activities ◽  
Testicular Function ◽  
Wide Range ◽  
The Impact

The detrimental effect of diclofenac sodium (Diclo-Na) on male reproductive organs is reported upon in this paper. Chitosan is a polysaccharide composed of various amounts of glucosamine. Chitosan nanoparticles (CH-NPs) have attracted much attention owing to their biomedical activity. Selenium (Se) has a vital role in nutrition, plays an important role in enhancing male reproduction, and has a wide range of free radical scavenging activities. However, the study of the impact of chitosan nanoparticles in combination with Se (IV) (CH-NPs/Se) on male reproductive toxicity associated with Diclo-Na administration is lacking in recent literature. The current study assessed the ameliorative effects of complexes of CH-NPs/Se (IV) on Diclo-Na and the ways in which they alter reproductive toxicity in male rats. Male rats were treated for 30 days successively, either with Diclo-Na (10 mg/kg) or co-treated with a CH-NPs/Se complex (280 mg/kg). Sperm characteristics, marker enzymes of testicular function, LH, FSH, and testosterone were evaluated in addition to oxidative stress markers and histological alterations. CH-NPs/Se significantly alleviated Diclo-Na-induced decline in sperm count and motility, testicular function enzymes, and levels of LH and testosterone in serum. Additionally, CH-NPs/Se co-administration at 280 mg/Kg, inhibited the Diclo-Na-induced decline of antioxidant enzyme activities and elevated oxidative stress indices and reactive free radicals in testicular homogenates of male rats. CH-NPs/Se (280 mg/kg) alone improved Diclo-Na and ameliorated histological damages in exposed rats. In conclusion, chitosan improved testicular function in Diclo-Na-treated rats by enhancing the testosterone hormone levels, ameliorating testicular tissue, and inhibiting markers of oxidative stress in male rats.

scholarly journals Neurological Alterations and Testicular Damages in Aging Induced by D-Galactose and Neuro and Testicular Protective Effects of Combinations of Chitosan Nanoparticles, Resveratrol and Quercetin in Male Mice

Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa
Keyword(s):  
Oxidative Stress ◽  
Chitosan Nanoparticles ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Wide Range ◽  
Neurological Alterations

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.

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.

Di(2-ethylhexyl)phthalate induces reproductive toxicity via JAZF1/TR4 pathway and oxidative stress in pubertal male rats

2019 ◽  
Vol 35 (3) ◽  
pp. 228-238 ◽  
Author(s):  
Yu-Qin Shi ◽  
Guo-Qing Fu ◽  
Jing Zhao ◽  
Shen-Zhou Cheng ◽  
You Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Morphological Changes ◽  
Reproductive Toxicity ◽  
Male Reproduction ◽  
Male Rats ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Cyclin A1 ◽  
Ethylhexyl Phthalate ◽  
Dehp Exposure ◽  
And Oxidative Stress

Di(2-ethylhexyl)phthalate (DEHP) is a typical endocrine-disrupting chemical and reproductive toxicant. Although previous studies have attempted to describe the mechanism by which DEHP exposure results in reproductive dysfunction, few studies focused on puberty, a critical period of reproductive development, and the increased susceptibility to injury in adolescents. To elucidate the mechanism underpinning the testicular effects of DEHP in puberty, we sought to investigate the JAZF1/TR4 pathway in the testes of pubertal rats. Specifically, we focused on the role of the JAZF1/TR4 pathway in male reproduction, including the genes JAZF1, TR4, Sperm 1, and Cyclin A1. In the present study, rats were exposed to increasing concentrations of DEHP (0, 250, 500, and 1000 mg/kg/day) by oral gavages for 30 days. Then we assayed testicular zinc and oxidative stress levels. Our results indicated that DEHP exposure could lead to oxidative stress and decrease the contents of testicular zinc. Additionally, significant morphological changes and cell apoptosis were observed in testes exposed to DEHP, as identified by hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase-mediated nick and labeling assay. By measuring the expression levels of the above relevant genes by qPCR, we found the DEHP-induced increased expression of JAZF1 and decreased expression of TR4, Sperm 1, and Cyclin A1. Therefore, we have demonstrated that in vivo exposure to DEHP might induce reproductive toxicity in pubertal male rats through the JAZF1/TR4 pathway and oxidative stress.

scholarly journals Zinc Oxide Nanoparticles Improve Testicular Steroidogenesis Machinery Dysfunction In Benzo [α] Pyrene Challenged Rats

2021 ◽  
Author(s):  
Niveen M. Daoud ◽  
S Aly Mohamed ◽  
Omaima H. Ezzo ◽  
Naglaa A. Ali
Keyword(s):  
Oxidative Stress ◽  
Zinc Oxide ◽  
Zinc Oxide Nanoparticles ◽  
Male Reproduction ◽  
Male Rats ◽  
Oxide Nanoparticles ◽  
Zno Nps ◽  
Positive Effects ◽  
Defensive Role ◽  
The Impact

Abstract Although Zinc oxide nanoparticles (ZnO NPs) in low doses have potentially positive effects on reproduction by their antioxidant effects, the defensive role of Zinc nanomaterials against environmental pollutants that affect male reproduction has not been adequately studied. We designed our study to assess the impact of ZnO NPs towards reproductive dysfunction induced by Benzo[α]Pyrene (B[a]P). Forty-eight mature male rats were randomly distributed into six equal groups: G1; negative control, G2&3- positive control I &II (either 10 or 30 mg ZnO NPs / kg BW); G4. (150 mg Bap / kg BW), G 5 & 6 (Co- administrated B[a]P with different concentrations of ZnO NPs). Oxidative stress biomarkers, semiquantitative real-time PCR for steroidogenic enzymes (CY11A1, StAR, and 3β- HSD), testosterone levels and histopathology in the liver, kidney, and testicles were examined for this investigation. B[a] P treated group showed significant deterioration in all reproductive parameters and induced oxidative stress. Co-administration ZnO NPs eased oxidative stress and effectively increased the expression of CY11A1, StAR, and 3β- HSD and improved histopathological changes in the examined organs. Our results using the selected doses and with Nano particle properties confirm that ZnO NPs have an obvious ameliorative effect against B[a] P.

scholarly journals Eugenol attenuates concanavalin A-induced hepatitis through modulation of cytokine levels and inhibition of mitochondrial oxidative stress

2019 ◽  
Vol 71 (2) ◽  
pp. 339-346
Author(s):  
Jing Liu ◽  
Yidong Mao
Keyword(s):  
Oxidative Stress ◽  
Concanavalin A ◽  
Hepatoprotective Activity ◽  
Antioxidant Enzyme Activities ◽  
Mitochondrial Oxidative Stress ◽  
Immune Mediated ◽  
Wide Range ◽  
Cytokine Levels ◽  
Glucose 6 Phosphate Dehydrogenase

Therapeutic management of hepatitis with conventional drugs alone worsens hepatic functioning in the long term because of sustained oxidative stress. Active compounds from several plant sources have been investigated to counteract this. Eugenol, a phytochemical abundant in various plants, is known for its wide range of pharmacological effects. There is a lacuna in the deeper understanding of its hepatoprotective activity at the molecular level. Our present study aimed to determine the effects of eugenol on the changes in antioxidant components, inflammatory cytokines and modulation of mitochondrial oxidative stress in immune-mediated hepatitis. We employed a model that mimics viral hepatitis using concanavalin A (ConA) to induce T-cell-mediated acute hepatitis. Eugenol increased (P<0.01) antioxidant enzyme activities, including reduced glutathione (GSH)-regenerating enzyme, glutathione reductase, and glucose-6-phosphate dehydrogenase. Its antiinflammatory and antifibrogenic effects were evident from the reduction (P<0.01) in interleukin and tumor necrosis factor levels. Eugenol was found to decrease mitochondrial oxidative stress, which was elevated in hepatitis. The hepatoprotective effects of eugenol were confirmed by histological findings. The current investigation shows that eugenol exerts a hepatoprotective effect through the modulation of different pathways which include restoration of mitochondrial oxidative stress. Eugenol could be a promising candidate for human hepatitis management, warranting preclinical studies.

scholarly journals Pesticides as endocrine distruptors of the reproductive system (literature review and own research)

2021 ◽  
pp. 49-62
Author(s):  
Ninel Shepelska ◽  
Mykola Prodanchuk ◽  
Yana Kolianchuk
Keyword(s):  
Reproductive Health ◽  
Endocrine Disruptors ◽  
Reproductive System ◽  
Reproductive Toxicity ◽  
Endocrine System ◽  
Reproductive Function ◽  
Dose Dependence ◽  
Animal Cells ◽  
Wide Range ◽  
The Impact

Currently, one of the main threats to human health is undoubtedly endocrine disruptors (ED), since they directly disrupt the processes of homeostasis maintenance, controlled by the endocrine system, the purpose of which is to maintain normal functions and development in a constantly changing environment. Pesticides can disrupt the physiological functioning of many endocrine axes, including the endocrine mechanisms that ensure reproductive health. It should be noted that research aimed at preventing chemically induced reproductive disorders in the human population is one of the central areas of preventive medicine, both in terms of their importance and the complexity of the tasks being solved. Analysis and generalization of the results of our own long-term studies have shown that the selective, and, therefore, the most dangerous toxicity of pesticides for the reproductive system is determined by endocrine-mediated mechanisms of etiopathogenesis. The low level of doses inducing pathological changes in reproductive function in our studies fully confirms one of the universal signs inherent in endocrine-distruptive compounds. The above examples demonstrate a wide range of possible endocrine-mediated mechanisms of reproductive toxicity of pesticides - endocrine disruptors. However, it is very important to note that low doses may be more effective in changing some endpoints compared to high (toxic) doses. Currently, several mechanisms have been identified and studied that demonstrate how hormones and ED induce non-monotonic reactions in animal cells, tissues and organs. The reproductive system, the functioning of which is ensured by a fine balancing of the action of androgens and estrogens, is one of the systems that presents a unique opportunity for modeling a non-monotonic dose dependence. All of the above indicates the extreme danger of the impact of hormonally active agents on the reproductive health of a person and his offspring. At the same time, the threat of endocrine-mediated disorders for subsequent generations can also be realized through the induction of mechanisms of development of epigenetic transgenerational effects. Taking into account the results of studies of the mechanisms of the ED destructive action, as well as their ability to induce non-monotonic dose dependence at an extremely low dose level, it should be admitted that, apparently, there is a need to revise the paradigm of methodological approaches to the regulation of pesticides with endocrine-disruptive properties. Key words: pesticides, endocrine disruptors, reproductive system

scholarly journals Roles of Moringa oleifera Leaf Extract in Improving the Impact of High Dietary Intake of Monosodium Glutamate-Induced Liver Toxicity, Oxidative Stress, Genotoxicity, DNA Damage, and PCNA Alterations in Male Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Tarfa Albrahim ◽  
Manal Abdulaziz Binobead
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Leaf Extract ◽  
Liver Toxicity ◽  
Monosodium Glutamate ◽  
Male Rats ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Glutamyl Transferase ◽  
The Impact

It is common for food to be made more palatable through the use of the flavour enhancer monosodium glutamate, also known as vetsin powder. The purpose of the study described in this paper was to explore how vetsin-induced hepatic toxicity, DNA fragmentation, damage, and oxidative stress modifications could be mitigated with moringa leaf extract (MLE). To that end, 40 male rats were separated into four groups: normal control, positive control or MLE, vetsin, and vetsin combined with MLE. Results indicated that, compared to the control group, the levels of serum alanine aminotransferase (ALT), aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), liver malondialdehyde (MDA), DNA damage, injury, PCNA, and P53 expressions were significantly enhanced by the administration of vetsin (P<0.05). However, the vetsin group had significantly reduced levels of albumin, globulin, total protein, liver glutathione (GSH), superoxide dismutase enzyme (SOD), catalase, and glutathione S-transferase (GST) enzyme activities (P<0.05) by comparison to control. Meanwhile, modifications in liver functions, oxidative stress, DNA damage, liver injury, and PCNA expression were alleviated when vetsin was administered alongside MLE. The authors conclude that vetsin may have many side effects and that MLE can ameliorate biochemical changes, oxidative stress, hepatic injury, PCNA, and P53 alterations induced by vetsin administration.

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