Quercetin attenuates di-(2-ethylhexyl) phthalate-induced testicular toxicity in adult rats

2015 ◽  
Vol 35 (3) ◽  
pp. 232-243 ◽  
Author(s):  
MF Abd-Ellah ◽  
HAA Aly ◽  
HAM Mokhlis ◽  
AH Abdel-Aziz
Keyword(s):  
Oxidative Stress ◽  
Corn Oil ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Prostatic Acid Phosphatase ◽  
Serum Testosterone Level ◽  
Testicular Toxicity ◽  
Group Vi ◽  
Adult Rats ◽  
Ethylhexyl Phthalate

The aim of the present study was to investigate the potential oxidative damage of di-(2-ethylhexyl) phthalate (DEHP) in the rat testis and to further elucidate the potential modulatory effect of quercetin. DEHP was diluted in corn oil and given to rats by oral gavage at doses 0, 300, 600, and 900 mg/kg/day (groups I, III, IV, or V, respectively) for 15 consecutive days. Group VI was pretreated with quercetin (90 mg/kg), 24 h before starting the experiment and then treated with DEHP (900 mg/kg/day) for 15 consecutive days. Group II was treated with quercetin (90 mg/kg/day). The relative testes weight and sperm motility were significantly decreased by treatment with 900 mg/kg of DEHP. Both sperm count and daily sperm production were significantly decreased by DEHP treatment at doses of 600 and 900 mg/kg. Serum testosterone level and prostatic acid phosphatase (ACP) activity and testicular lactate dehydrogenase-X (LDH-X) activity were significantly decreased in animals treated with 900 mg/kg. Serum total ACP activity was significantly increased in animals treated with 600 and 900 mg/kg of DEHP. DEHP treatment induced oxidative stress and histopathological abnormality. These abnormalities were effectively normalized by pretreatment with quercetin except for LDH-X near normalcy. In conclusion, the findings of this study demonstrate that DEHP impairs testicular function at least, in part, by inducing oxidative stress and quercetin has a potent protective effect against DEHP-induced testicular toxicity in rats.

Testicular toxicity of gentamicin in adult rats: Ameliorative effect of lycopene

2019 ◽  
Vol 38 (11) ◽  
pp. 1302-1313 ◽  
Author(s):  
HAA Aly
Keyword(s):  
Oxidative Stress ◽  
Histopathological Examination ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Testicular Toxicity ◽  
Adult Rats ◽  
Adult Rat ◽  
Gentamicin Treatment ◽  
Ameliorative Effect ◽  
Induced Apoptosis

The current study was aimed to investigate the ameliorative effect of lycopene against gentamicin-induced testicular toxicity in adult rat testes. Pretreatment with lycopene (4 mg/kg/day) significantly prevented the decrease in the absolute testes weight and relative testes weight and the reduction in sperm count, motility, viability, and daily sperm production in gentamicin (100 mg/kg/day)-treated rats. Gentamicin significantly decreased the level of serum testosterone and testicular lactate dehydrogenase-X and G6PDH activities but a marked increase was observed upon pretreatment with lycopene. Testicular caspase-3 and -9 activities were significantly increased but lycopene showed significant protection from gentamicin-induced apoptosis. Oxidative stress was induced by gentamicin treatment as evidenced by increased hydrogen peroxide level and lipid peroxidation and decreased the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities and glutathione content. These alterations were effectively prevented by lycopene pretreatment. Histopathological examination showed loss of spermatogenesis and morphological abnormalities of the testis after treatment with gentamycin. These abnormalities were effectively normalized by pretreatment with lycopene. In conclusion, gentamicin decreases rat testes weight and inhibits spermatogenesis. It induces oxidative stress and apoptosis by possible mitochondrial dysfunction. These data provide insight into the mode of action of gentamicin-induced testicular toxicity and the beneficial role provided by lycopene to restore the suppressed spermatogenesis.

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.

Evaluation of blood oxidant/antioxidant changes and testicular toxicity after subacute exposure to cadmium in albino rats: Therapeutic effect of Nigella sativa seed extracts

2020 ◽  
Vol 23 ◽  
Author(s):  
Ikenna Kingsley Uchendu ◽  
Henshaw Uchechi Okoroiwu
Keyword(s):  
Oxidative Stress ◽  
Testosterone Level ◽  
Nigella Sativa ◽  
Serum Testosterone ◽  
Seed Extract ◽  
Serum Testosterone Level ◽  
Albino Rats ◽  
Testicular Toxicity ◽  
Oral Group ◽  
Testicular Injury

Aim and Objective: Cells and tissues of the body are prone to oxidative damage as a result of increased level of reactive oxygen species and nitrogen radical beyond the detoxifying ability of the endogenous antioxidant system. This study aimed to evaluate the ameliorative effect of methanolic extracts of Nigella sativa (MENS) against cadmium-induced blood oxidative stress and testicular toxicity in albino rats. Materials and Methods: Twenty five (25) male albino rats, weighing (200±20g), were randomly grouped into five groups (A-E). Group B (Negative Control) received intraperitoneal administration of cadmium chloride (CdCl2, 5mg/kg) only, group C received CdCl2 and low dose MENS (300mg/kg, oral), group D received CdCl2 and high dose MENS (600mg/kg, oral), group E (Positive control) received CdCl2 and Vitamin C (200mg/kg, oral), for 14 days. No treatment was administered to group A (Normal control). The oxidative state of the blood was assessed by measuring the blood levels or activities of MDA, CAT, GSH and SOD; while testicular injury was assessed by measuring serum testosterone level using ELISA. The testes were harvested for histopathological examination. Results: The results showed that cadmium induced a marked elevation in the level of MDA, and a decrease in SOD, CAT and GSH levels or activities (p<0.05 or p<0.01); but no significant alteration in the serum testosterone level (p>0.05); Histopathological studies on the testes showed that cadmium significantly induced testicular injury, which was however ameliorated by the seed extract of N.sativa. Conclusion: We conclude that N.sativa seed extract is potentially testiculoprotective and attenuates oxidative stress against harmful chemical toxins such as cadmium.

scholarly journals The ameliorative effect of ellagic acid on di-(2-ethylhexyl) phthalate-induced testicular structural alterations, oxidative stress, inflammation and sperm damages in adult mice

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Azam Hosseinzadeh ◽  
Saeed Mehrzadi ◽  
Amir Siahpoosh ◽  
Zahra Basir ◽  
Nosrat Bahrami ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ellagic Acid ◽  
Nitrosative Stress ◽  
Inflammatory Responses ◽  
Corn Oil ◽  
Endocrine Disrupting Chemicals ◽  
Reproductive Toxicity ◽  
Primary Spermatocyte ◽  
Serum Testosterone ◽  
Ethylhexyl Phthalate

Abstract Background Phthalates such as di (2-ethylhexyl) phthalate (DEHP) are well known exogenous substances, disrupting reproductive system function and structure. The current research demonstrated the effect of ellagic acid (EA) on DEHP-induced testicular injury in mice. Methods Thirty-five healthy adult male mice were randomly divided to five groups; normal saline receiving group, DEHP (2 g/kg/day, dissolved in corn oil, p.o.) receiving group, DEHP (2 g/kg/day, dissolved in corn oil, p.o.) and EA receiving groups (25, 50 and 100 mg/kg/day, p.o.). Treatment duration of animals was 14 days. Body and testes weights and sperm characteristics and histological changes of testes were evaluated. Serum testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were analyzed. In the testicular tissue, oxidative/nitrosative stress markers and inflammatory cytokine levels were measured. Results Ellagic acid significantly reduced DEHP-induced reduction of body and testes weights. The DEHP-induced reduction of spermatogonia, primary spermatocyte and sertoli cells numbers as well as reduction of sperm vitality and progressive motility were reversed by EA. Furthermore, EA inhibited DEHP-induced alterations in serum hormone levels. These effects were associated with the reduction of DEHP-induced increased level of oxidative stress and inflammatory responses. Conclusions Ellagic acid considerably inhibits testicular toxicity of DEHP through reducing oxidative/nitrosative stress and inflammatory responses. Our data suggest that EA may be considered as a promising agent to inhibit male reproductive toxicity induced by endocrine disrupting chemicals such as DEHP.

scholarly journals Gentamicin and amikacin adversely affect male infertility indicated by pharmacological, andrological and pathological evidence

2020 ◽  
Vol 9 (2) ◽  
pp. 218
Author(s):  
Hozaifa K. Elsawah ◽  
Mohamed M. Kandiel ◽  
Aziza A. Amin ◽  
Haitham M. Mokhimar ◽  
AbuBakr M. El Mahmoudy
Keyword(s):  
Male Infertility ◽  
Therapeutic Dose ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Reproductive Organs ◽  
Serum Testosterone Level ◽  
Double Dose ◽  
Medication History ◽  
The Third ◽  
Significant Difference

Background: Many drugs are implicated in male infertility and screening for medication history is an important for diagnosis and treatment of the problem. The aim is to study amikacin effect on male reproductive system in comparison to gentamicin.Methods: Twenty-five male wister rats weighted 220±20 gm and aged 8 weeks were randomly divided into five groups of five. The first group received gentamicin in dose 18.25 mg/kg/day once daily (OD) (therapeutic dose). The second group received gentamicin with double dose of the first group. The third group received amikacin in dose 54.75 mg/kg/day OD (therapeutic dose). The Fourth group received amikacin with double dose of the third group. However, the fifth group served as a control and received normal saline (NS) OD. All treatments were administered intraperitoneally (IP) for 14 days. On the 15th day, blood samples and reproductive organs were obtained from all animals. Testicular tissues were prepared for genetic testing and chemical and microscopical examination.Results: Amikacin and gentamicin negatively affected reproductive organs weights, sperm parameters, serum follicle stimulating hormone and luteinizing hormone (LH) level relative to control (p<0.05). However, serum testosterone level was only affected with gentamicin (p<0.05). A significant difference between gentamicin and amikacin was found in sperm count, testis and epididymis weights and serum testosterone and LH level (p<0.05). Testicular histopathological changes were also found with the two drugs with different degrees. Effects of both gentamicin and amikacin were dose-dependent.Conclusions: Both gentamicin and amikacin adversely affect andrological function that should be monitored and controlled during application of these drugs.

scholarly journals Aluminium phosphide-induced testicular toxicity through oxidative stress in Wistar rats: Ameliorative role of hesperidin

2018 ◽  
Vol 2 ◽  
pp. 239784731881279 ◽  
Author(s):  
Olusegun Kayode Afolabi ◽  
Adedoja Dorcas Wusu ◽  
Regina Ugbaja ◽  
John Olabode Fatoki
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Sperm Count ◽  
Sperm Parameters ◽  
Lipid Hydroperoxides ◽  
Testicular Toxicity ◽  
Testicular Damage ◽  
Histological Alterations ◽  
Aluminium Phosphide

The present study was designed to investigate aluminium phosphide (ALP)-induced testicular toxicity, including its effects on sperm parameters and histological alterations in Wistar rats, and the possible protective role of hesperidin (HSD). Oral administration of ALP at 1.15 mg/kg body weight (1/10 LD50) for 30 days resulted in a significant increase in testicular malondialdehyde, lipid hydroperoxides, and oxidized protein levels. These indicators of oxidative stress were accompanied by decreased activity of the antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase, followed by a drastic reduction in the non-enzymatic antioxidant indices of glutathione and total antioxidant capacity when compared to control. Furthermore, ALP treatment produced a marked reduction in sperm count, motility and viability while increasing abnormal sperm morphology and adverse histopathological changes in testis. Co-administration with HSD significantly ameliorated ALP-induced testicular damage by suppressing oxidative stress indices and enhancing antioxidant status while also improving the sperm parameters and histological alterations in ALP-treated rats. The results of the present study indicated that testicular toxic effects of ALP are due to oxidative imbalance and that HSD could be a potential therapeutic agent against ALP-induced testicular damage.

scholarly journals Sulforaphane response on aluminum-induced oxidative stress, alterations in sperm characterization and testicular histomorphometry in Wistar rats

2020 ◽  
Author(s):  
Babatunde Ogunlade ◽  
Sunday Adelakun ◽  
Kingsley Iteire
Keyword(s):  
Oxidative Stress ◽  
Adult Male ◽  
Antioxidant Status ◽  
Wistar Rats ◽  
Sperm Count ◽  
Seminiferous Tubules ◽  
Testicular Toxicity ◽  
Significant Difference ◽  
Male Wistar Rats ◽  
Aluminum Trichloride

Background: The exposure of male individual to environmental toxicant is regarded as a channel that results in reduced sperm counts and infertility. Objective: This study investigated the ameliorative response of Sulforaphane (SFN) on Aluminum trichloride (AlCl3) induced testicular toxicity in adult male Wistar rats. Materials and Methods: A total of 32 adult male Wistar rats (180-200 gm between 8-10 wk) were divided into four groups (n = 8/each). Group A) received distilled water orally as placebo; Group B) received 100 mg/kgbw AlCl3 only orally; Group C) received 100 mg/kgbw AlCl3 and 100 mg/kgbw SFN orally; and Group D) received 100 mg/kgbw SFN only orally. After 28 days of experiment, animals underwent cervical dislocation, blood serum was obtained for analysis, and testes were harvested for biochemical assays, histology, hormonal profile, and sperm characterization. Results: The sperm parameters showed a significant difference within the AlCl3 only group compared with the control and SFN only groups (p = 0.02). However, AlCl3 and SFN co-treatment showed improvement in the motility, viability, and sperm count compared with the AlCl3 only group (p = 0.02). Furthermore, there was a significant decline in the levels of hormones profile and antioxidant status in AlCl3 only group compared to the control and SFN only (p = 0.02). The testicular histoarchitecture of the AlCl3 only group showed shrinkage of seminiferous tubules, spermatogenesis disruption, and empty lumen compared to the control and SFN only groups. Conclusion: The present study revealed the ameliorative response of SFN on AlCl3-induced testicular toxicity on serum hormone profiles, antioxidant status, lipid peroxidation, and histomorphometric analysis through oxidative stress. Key words: Sulforaphane, Aluminum trichloride, Oxidative stress, Testis, Histology.

scholarly journals Molecular, Immunomodulatory, and Histopathological Role of Mesenchymal Stem Cells and Beetroot Extract on Cisplatin Induced Testicular Damage in Albino Rats

Animals ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 1142
Author(s):  
Marwa T. Hassen ◽  
Hanaa K. Mohamed ◽  
Metwally M. Montaser ◽  
Mohamed E. El-Sharnouby ◽  
Nabil Awad ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Sperm Count ◽  
Combined Treatment ◽  
Regulatory Protein ◽  
Serum Testosterone Level ◽  
Control Group ◽  
Albino Rats ◽  
Testicular Toxicity ◽  
Testicular Damage

Cisplatin (Cis) a drug commonly used as a chemotherapeutic agent to treat various types of cancer, inducing testicular damage. The present study aimed to investigate the inhibitory potential of bone marrow-derived mesenchymal stem cells (BM-MSCs) and beetroot extract (BRE) in albino rats after testicular toxicity induced by cisplatin. Thirty adult male albino rats were grouped into: the control group, Cis group receiving a single dose of 7 mg/kg i.p. (intraperitoneal) to induce testicular toxicity, Cis plus BM-MSCs injected Cis followed by 2 × 106 of BM-MSCs; Cis plus BRE group receiving Cis followed by 300 mg/kg body weight/day of BRE, and Cis plus BM-MSCs and BRE group. In the current study, Cis reduced sperm count, serum testosterone level, and testicular activity of alkaline phosphatase (AKP), besides a marked inhibition of succinate dehydrogenase (SDH) activity. In addition, it significantly increased malondialdehyde (MDA) and along with a marked decrease in testis reduced glutathione content and total antioxidant capacity (TAC). At the same time, Cis administration resulted in a marked elevation in interleukine-6 and the iNOS and caspase-3 genes; however, it decreased the expression of steroidogenic acute regulatory protein (StAR). Combined treatment with BM-MSCs and BRE resulted in great improvement of all previous parameters. These results were also confirmed by histopathological and immunohistochemical examination. In conclusion, both MSCs and BRE were found to have potent potentials to inhibit testicular damage induced by cisplatin.

Repeated administration of ethambutol in therapeutic dose causes testes alteration and spermatogenesis disruption in Wistar rats

2016 ◽  
Vol 36 (5) ◽  
pp. 520-533 ◽  
Author(s):  
GM Shayakhmetova ◽  
LB Bondarenko ◽  
AK Voronina ◽  
AV Matvienko ◽  
V Kitam ◽  
...  
Keyword(s):  
Computer Simulation ◽  
Messenger Rna ◽  
Sperm Count ◽  
Direct Interaction ◽  
Serum Testosterone ◽  
Repeated Administration ◽  
Male Rats ◽  
Testicular Toxicity ◽  
The Impact

Ethambutol (EMB) is conventionally used to treat tuberculosis and atypical Mycobacterium infections in combination with other antimycobacterial drugs. Eventually, EMB testicular toxicity has not been explored extensively yet. The aim of the study is to evaluate testicular toxicity of EMB. We explored the impact of EMB on male rats’ fertility, testosterone level and germ cells state, testicular pro- and anti-oxidant status and DNA damage, as well as identified EMB effects on cytochrome P-450 2E1 (CYP2E1) both with computer simulation and in vivo. We demonstrated that EMB administration to male rats decreased in epididymal sperm count (19%) and fertility index (53%). These events were accompanied by reduction in serum testosterone content (1.6 times) and appearance of spermatogenic epithelium damages. It was also found in testes the intensification of lipid peroxidation, decrease in reduced glutathione content and changes in DNA fragmentation. Additionally, computer simulation showed direct interaction of EMB with CYP2E1 active site and heme. On the top of this, we demonstrated that level of testicular CYP2E1 messenger RNA in EMB-treated rats was increased 8.7 folds and p-nitrophenol hydroxylase activity in testes rose three folds. As this shows, EMB-caused CYP2E1 induction, oxidative stress, and apoptosis in the testes contribute to inhibition of steroidogenesis enzymes and spermatogenesis disruption.

scholarly journals Prepubertal Exposure to Genistein Alleviates Di-(2-ethylhexyl) Phthalate Induced Testicular Oxidative Stress in Adult Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Lian-Dong Zhang ◽  
He-Cheng Li ◽  
Tie Chong ◽  
Ming Gao ◽  
Jian Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Adult Rats ◽  
Environmental Endocrine Disruptors ◽  
Sprague Dawley Rats ◽  
Antioxidative Effects ◽  
Testicular Histology ◽  
Ethylhexyl Phthalate

Di-(2-ethylhexyl) phthalate (DEHP) is the most widely used plastizer in the world and can suppress testosterone production via activation of oxidative stress. Genistein (GEN) is one of the isoflavones ingredients exhibiting weak estrogenic and potentially antioxidative effects. However, study on reproductive effects following prepubertal multiple endocrine disrupters exposure has been lacking. In this study, DEHP and GEN were administrated to prepubertal male Sprague-Dawley rats by gavage from postnatal day 22 (PND22) to PND35 with vehicle control, GEN at 50 mg/kg body weight (bw)/day (G), DEHP at 50, 150, 450 mg/kg bw/day (D50, D150, D450) and their mixture (G + D50, G + D150, G + D450). On PND90, general morphometry (body weight, AGD, organ weight, and organ coefficient), testicular redox state, and testicular histology were studied. Our results indicated that DEHP could significantly decrease sex organs weight, organ coefficient, and testicular antioxidative ability, which largely depended on the dose of DEHP. However, coadministration of GEN could partially alleviate DEHP-induced reproductive injuries via enhancement of testicular antioxidative enzymes activities, which indicates that GEN has protective effects on DEHP-induced male reproductive system damage after prepubertal exposure and GEN may have promising future in its curative antioxidative role for reproductive disorders caused by other environmental endocrine disruptors.

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