The current study investigated the protective effect of sesame seed oil (SSO) against testicular damage and endocrine disruption induced by the oral intoxication with penconazole (PENZ), a commonly used systemic triazole fungicide, in adult male Wistar rats. Subchronic oral exposure to two different doses of PENZ significantly reduced fertility indices, serum luteinizing hormone, follicle stimulating hormone, triiodothyronine and thyroxine levels, and by contrast a significant increase was recorded in serum estradiol and testosterone levels. Furthermore, PENZ significantly depleted testicular vitamins (A, C and E) level. On the other hand, administration of SSO prior to PENZ intoxication ameliorated most of the fertility indices and minimized PENZ-induced adverse effects on serum sexual, reproductive and thyroid hormones, compared to PENZ-treated animals. Histological data confirmed the biochemical findings. In conclusion, supplementation of SSO might be beneficial against the endocrine-disrupting potential and testicular toxicity induced by PENZ in adult male rats.
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The concurrent exposure of more than one environmen- tal toxicant in mammals induce depletion in antioxidant defence system as indicated with reduced levels of total thiols (TTH) including reduced glutathione (GSH). Anti- oxidant defence system scavenges reactive oxygen/nitrogen species (ROS/RNS) generated in tissues and sub-cellular compartments during intoxication . It has been reported that excessive generation of these free radicals in testicular tissue reduces antioxidant defence resulting in the disruption of the functional integrity of membrane struc- tures of mitochondria and other cytoplasmic organelles through peroxidation of phospholipids, proteins and nucle- otides [12, 13]. Hence, ROS plays an important role in the pathogenesis of male reproductive system due to the existence of high polyunsaturated fatty acid (PUFA) in the testes which makes it more sensitive to oxidative insults [14, 15]. Therefore, the present study was aimed to evaluate the potentiating effect of imidacloprid (IMI) on arsenic-in- duced testicular toxicity in male Wistar rats.
was used compared to what was reported in earlier literature. In addition, the effects of melatonin on testicular toxicity of the model were investigated. Lipid peroxidation has been implicated in the pathogenesis of hepatic injury by the free radical derivatives of CCl 4 and is responsible for cell membrane damage and the consequent release of marker enzymes of hepatotoxicity. In this study, significantly elevated levels of MDA, products of membrane lipid peroxidation observed in CCl 4 -treated rats indicated hepatic damage. Pre-treatment with melatonin reduced lipid peroxidation, which could be attributed to the radical scavenging antioxidant constituents. GSH is the major non-enzymatic antioxidant and regulator
were killed, dissected, then blood and testis samples were collected for biochemical and stereological parameters analysis. The data were analyzed by SPSS-21 software. G. tournefortii at all doses (especially GT40) and glibenclamide significantly (p≤0.05) ameliorated the concentrations of fasting blood glucose, testosterone, superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase. Also, multiple doses of G. tournefortii (especially GT40) and glibenclamide increased the weight and volume of the testis, the volumes of the tubule and interstitial tissue, the length and diameter of the tubule, the height of the germinal epithelium, and the number of the Leydig cell compared to the diabetic untreated group. According to the obtained results, G. tournefortii aerial parts aqueous extract can regulate the concentrations of biochemical parameters and inhibit testicular damages in alloxan monohydrate induced diabetic mice. It seems that G. tournefortii can be offered as a testicular protective supplement or drug for prevention, control, and treatment of testicular toxicity in diabetic patients.
Increasing awareness has been lately paid to the toxicity of synthetic additives used in food. The main aim of this study was to survey the renal and testicular toxicity of synthetic food dye brilliant blue. Administration of the brilliant blue (BB) changed body and relative organs weights, serum creatinine, urea (BUN), uric acid and serum FSH, LH, testosterone levels. This study proved that BB induced oxidative damage as manifested by significant increase in Lipid peroxidation with disorganization in the activity of glutathione peroxidase, protein carbonyl and reactive oxygen species content. Histopathological changes include: infiltration and vacuolation in kidney. In addition; degeneration and necrosis of spermatogoneal cells lining seminiferous tubules in testis. Furthermore; BB induced appotosis via activation of casp-3. Administration of curcumin with BB attenuated the cytotoxic effects of brilliant blue on kidney and testis tissues and reducing apoptotic cell death as well as improved the redox status of kidney and testis.
Montelukast treatment reversed the decreased effect of etoposide on serum testosterone levels. To the best of our knowledge, there was no study about the effects of montelukast treatment on male fertility with etoposide treatment, however, it is thought that this effect of etoposide may occur through interference with LH receptor expression, impairment of the cholesterol mobilization to mitochondrial cytochrome P450, or reduction of the activity of this enzyme, thus interfering with the first steps in testosterone production (Silici et al., 2009). Additionally, the current study showed that montelukast significantly increased sperm count, motility and viability in etoposide-treated rats. Previously, spermatological effects of montelukast did not examined with etoposide. Montelukast treatment might be beneficial due to its antioxidant, anti-inflammatory and antipoptotic properties and may be positively affect etoposide-induced infertility. In the histopathological evaluation, histological damage was decreased when montelukast was combined with etoposide. It was considered that the histopathological effects may attribute to the imbalance between oxidant and antioxidant status and/or increased inflammation and DNA damage in testes tissue induced by etoposide that may contribute also to male infertility by reducing sperm count. For this reason, a decrease 61431 Abeer I. Abd El-Fattah et al. Pretreatment with montelukast and curcumin protect against testicular toxicity in rats:
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According to Indian Systems of Medicine, Crossandra infundibuliformis (L.) belonging to the family (Acanthaceae), were used for treating male sexual disorders since ancient times. Aim of this study to evaluate the phytochemical constituents and the aphrodisiac potential of the petroleum ether extract of leaves of Crossandra infundibuliformis (L.) on ethanol induced testicular toxicity in albino wistar rats. Phytochemical screening revealed the presence of alkaloids and saponins. All the doses resulted in significant increase in mount frequency, intromission frequency and significantly prolonged the ejaculatory latency (P < 0.05) and reduced mount and intromission latency (P < 0.05). There was also a significant increase in serum testosterone concentrations in all the groups in a manner suggestive of dose-dependence (P < 0.05). Results of this study concluded that the petroleum ether extract of Crossandra infundibuliformis (L.) increased the blood testosterone concentrations and this may be the mechanism responsible for its aphrodisiac effects and various masculine behaviors. It may be used to modify impaired sexual functions in animals, induced testicular toxicity in albino wistar rats.
at 150 mg/kg bw for 15 days. The activities of the stress indicating enzymes (SOD, CAT) and MDA content as a result of LPO along with the total tissue protein and cholesterol were assessed in the testicular homogenate of rats. A significant reduction in the activities of SOD and CAT with parallel significant upsurge in MDA accompanied by a significant reduction in total tissue protein content and a significant rise in tissue cholesterol was observed in rat testes. Also, the reduction in the testicular weights along with a decline in testosterone concentration was detected. Further, Cur supplementation with Cd significantly upturned the Cd-induced variations in oxidative stress indicating enzymes and amended the testosterone levels, total testicular protein, and cholesterol content. Therefore, it can be concluded that Cur plays a protective role against testicular toxicity produced by a single dose of CdCl 2 .
Cancer chemotherapies have been associated with many adverse effects including infertility, which has emerged as an issue of growing importance issues worldwide. 1 Doxorubicin (DOX) is one of the anthracycline antibiotics that are widely used for the treatment of various types of malignancies including breast cancer, bladder cancer, and lymphoma. It mainly interacts with DNA by intercalation leading to inhibition of the progression of topoisomerase II enzyme, thus inhibiting DNA replication. 2 Generation of reactive species is another mechanism of the cytotoxic effect of DOX. Additionally, it produces pronounced DNA damage through histone separation from the active chromatin. 3 The mechanism that is responsible for the testicular toxicity of DOX is not yet completely clear, but new studies often suggest
a previous research . Morel et al.  found that Leydig cells’ morphology is altered with disrupted chromatin followed by reduction in the cell number and is irreversibly substituted by inflammatory cells and this agreed with the current findings that are supported by the immunomarkers increased expres- sion. It is noted that fenugreek consumption restored serum testosterone level and testicular weight . The fenugreek being an antioxidant, it performs a cru- cial role in restoring testosterone level by eliminating ROS which is known to stop steroidogenesis [45, 60]. The cell type that is damaged is mainly in the early stage of spermatogenesis and the degree of germ cell damage is related to the dose of Cd exposure . This is consistent with the current findings that the spermatogonia are the primary cells that are affected. In contrast, another researcher observed that the exfoliated sloughed germ cells were spermatocytes and spermatids .
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In our previous studies [45, 46] we have shown that DCA induced oxidative stress in liver and renal tissues by affecting endogenous antioxidant defense enzymes and lipid peroxidation. In the same way, in this study, we found that DCA induced oxidative stress in testicular tissues illustrated by an alteration in antioxidant enzymes activity and in lipid peroxidation level beside a decrease in GSH level. Antioxidant enzymes represent a defense mechanism, and are responsible for detoxifica- tion of reactive oxygen species (ROS). The SOD–CAT system provides the first defense against oxygen toxicity. SOD is considered to be one of the most active enzymes, its activity is sufficient for the dismutation of superoxide anions to hydrogen peroxide (H 2 O 2 ) produced during
Diacetyl (Artificial Butter Flavoring) is used as an aroma carrier for foods And therefore, it is considered to be used by the food industry for adding aroma in several types of food products. The goal of this study was to investigate how artificial butter flavoring can affect the brain in terms of neurotransmissions, level of testosterone and histological changes in the testes of albino rats. It was dissected brain to measure neurotransmitters and testicular to histological study. The results of the study indicated that daily diacetyl consumption at 25 mg/kg b.wt was responsible for decreasing dopamine (DA), gamm-aminobutyric acid (GABA) along with serotonin (5-HT) and norepinephrine(NE) levels in different parts of the brain. The back of testicular tissue condition is regularly associated with lower testosterone hormonelevel confirmed histological changes in the testis necrosis of some cells , a significant decrease sperm mature and the tubular deficit. It can be concluded that diacetyl has sparked neurotoxicity and damagethe testicular tissue..
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toxicity in testes of rats, used as an animal model. Guidelines of National Institutes of Health, Islamabad were strictly followed in order to conduct experiments effectively. The designed protocol (Bch#248) was then approved by the Ethical Committee of Quaid-i-Azam University, Islamabad, Pakistan. Animals were kept at room temperature (25 ± 3 °C) with a 12 h dark/light cycle in ordinary cages. Animals were properly fed on standard laboratory feed and water.
Chlorpyrifos is activated in vivo to their oxygen analogs chlorpyrifos oxon mainly by enzymes of cytochrome P450 family. These oxidized metabolites are highly toxic but can be detoxiﬁed by esterases such as PON1. Thus, higher activity of paraoxonase enzyme in serum originates increased dialkyl phosphate levels in urine and decreased levels of the substrates (oxon forms), which in turn results in reduced toxicity of these oxon-metabolites.  Therefore the present results concerning that the increased level of PON1 activity towards diazoxon elicited a reduced effect of CPF metabolites on the organs functions, are consistent with the higher metabolicability to detoxify some organophosphates when higher enzyme activity occurs.
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Oral administration of cyclophosphamide in a daily single dose (5mg/kg of b.wt) to rats for 6 weeks induced significant (P< 0.05) decreases in body weight gain, food intake and feed efficiency ratio (FER), compared with the negative control rats (normal rats). Oral administration of Walnut seeds extract (WSE) and/or, vitamin E; and their combination to rats inflicted with testicular damage caused significant (P<0.05) increases in body weight gain, food intake and FER compared with the positive control group. There was a marked increase in body weight gain, feed intake and feed efficiency ratio in treated rats with a mixture of the WSE and vitamin E as recorded in Table 1.
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Overall, these inhibitory effects of lead on various enzymes would probably result in impaired antioxidant defenses by cells and render cells more vulnerable to oxidative stress. After the treatment with T. terrestris root extract and Vitamin C, GSH level was improved. In this study, administration of lead acetate showed elevation in testicular acid phosphatase activity and a significant (p<0.01) decrease in testicular alkaline phosphatase activity which reflects testicular degeneration, which may likely be a consequence of suppressed testosterone and indicative of lytic activity .
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testosterone with the increased levels of FSH and LH in experimental rats represented a damaged pituitary- testicular axis. According to Wang et al, a reduction in testosterone level could be explained by an increase in cortisol concentration that might suppress the Leydig cells through binding to the GC receptors on the cell surface (26). Our results demonstrated that GSE can improve the reproductive hormone (i.e., testosterone, FSH, and LH) levels in the Dex mice. This might be due to the protective effect of GSE on Leydig cells (8). In line with our findings, previous research approved the protective effects of GSE by using properties such as anti-apoptotic, anti-oxidative, and antigenotoxic (27). In addition, several researchers like Abarikwu et al, Hawkley et al, and Enyeart et al reported that GSE inhibited cortisol secretion by suppressing adrenocorticotropic hormone and increasing mRNAs coding for steroid controlling proteins (28-30).
Histopathological and morphometric results from this experiment indicate a significant reduction in the tubular and epithelial areas in the testis of methotrexate treated mice in comparison to controls and Omega-3 fatty acids -treated rats. These results also mirror other testicular parameters that were measured and further alludes that methotrexate induced damage may be via Sertoli cell destruction since the nutritional and structural support of germ cells are maintained by Sertoli cells.
results clearly demonstrates that lead acetate exposure can seriously alter the testes and reproductive function of adult male rats. Oxidative stress parameters were examined in testicular homogenate, and lipid peroxida- tion as measured by the amount of MDA was signifi- cantly (p < 0.05) elevated in the testes of lead treated rats (Table 1). Lipid peroxidation has been implicated in the aetiology of damage to subcellular membranes by inactivating cell constituents through oxidation or causing oxidative stress by undergoing radical chain re- action . The stimulation of lipid peroxidation, seemingly caused by lead treatment is related to the formation of free radicals after depletion of antioxi- dants. Table 1, shows a significant (p < 0.05) decline in the production of glutathione in the testes of lead exposed animals, as well as lead alteration in the func- tion of some antioxidant enzymes markers. Lead expos- ure resulted in a significant (p < 0.05) decrease in superoxide dismutase and catalase enzyme activities in the testes of the rats. This observations are similar to those made by Salawu et al., . Our study also showed that there was a significant (p < 0.05) increase in the levels of nitric oxide content in the testes of the animals similar to observations made by Moniem et al., . All these culminate to a depletion of total antioxi- dant content and an increase in reactive oxidant specie. Vigeh et al.,  describes lead’s ability to elevate ROS in biological systems as correlated to its active inhib- ition of sulfhydryl antioxidants synthesis, inhibition of enzyme reactions, damage to nucleic acids and inhib- ition of DNA repair. As such our results indicate that
The current study depicted the low level of acetyl- cholinesterase in malathion-treated group. These results are similar to the previous researchers who stated that pseudocholinesterase and acetylcholinesterase activity have been inhibited by the organophosphorus pesticides in the body tissues (John et al. 2001; Kalender et al. 2006; Rubin et al. 2002). These changes depend on con- centration and intensify with longer exposure. The ef- fects of malathion and other OPs may be at least partially because of they are able to cross the blood– testis barrier and enhance oxidative stress and peroxida- tion of lipids causing damage to the testes (Uzunhisar- cikli et al. 2007). Malathion does not directly inhibit action of the acetylcholinesterase before it is biotrans- formed. The toxicity to mammals of organophosphorus pesticides as malathion depends on mixed function oxi- dase (MFO) induced activation to its analogous oxygen correspondent, which directly inhibit acetylcholinester- ase (Pope 1999). Therefore, biological effects of mala- thion can be due to electrophilic attack on the cells with concomitant production of reactive oxygen species (Johnson et al. 2000). Therefore, the harmful effects of malathion on reproductive system of male mice may be due to its electrophilic attack on their cells.
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