Testicular Toxicity In Rats Research Articles

Aqueous extract of bay leaf (Laurus nobilis) ameliorates testicular toxicity induced by aluminum chloride in rats.

Human exposure to aluminum is inevitable, and one of the most adverse health effects of aluminum is a decrease in male fertility rates. Therefore, this study investigated the ameliorative effects of an aqueous extract from Laurus nobilis-bay leaf (BL) on aluminum chloride (AlCl3)-induced testicular toxicity in rats. Twenty-four Wistar rats were divided into four groups (n = 6, each group): The control (group 1) received normal saline; Group 2 animals were intraperitoneally administered with 30 mg/kg body weight (BW) AlCl3; and Groups 3 and 4 were co-administered AlCl3 with 125 or 250 mg/kg BW of BL extract, respectively, for 21 days. Testes, epididymis, and blood samples were collected. Testicular plasma enzyme activity was measured using a spectrophotometric assay, while concentrations of inflammatory biomarkers were determined using enzyme-linked immunosorbent assay kits. There was a significant increase (p < 0.05) in testicular enzyme activity in the group treated with AlCl3. However, there was no significant (p > 0.05) difference in testicular enzyme activity in groups co-administered AlCl3 and BL extract as compared with that in control. There was a significant (p < 0.05) increase in testicular nitrite concentration in the AlCl3-treated group, whereas the administration of BL extract significantly (p < 0.05) decreased nitrite concentration in Groups 3 and 4. Furthermore, the administration of BL extracts increased sperm count and improved the morphology of the testes in AlCl3-treated rats. Flavonoids, phenolic compounds, alkaloids, tannin, glycosides, saponin, anthraquinones, and steroids were identified in BL extract, with alkaloids and glycosides being the most abundant. Aqueous extract from BL ameliorated the toxic effect of AlCl3 and exhibited anti-inflammatory properties by inhibiting nitrite production while improving sperm count and morphology in AlCl3-treated rats. The bioactivity of the extract may be attributed to the presence of a wide range of phytochemicals. Therefore, BL aqueous extract could be a promising source of novel compounds with male fertility-promoting and anti-inflammatory properties.

α-Bisabolol Attenuates NF-κB/MAPK Signaling Activation and ER-Stress-Mediated Apoptosis by Invoking Nrf2-Mediated Antioxidant Defense Systems against Doxorubicin-Induced Testicular Toxicity in Rats.

The present study investigated the effects of α-bisabolol on DOX-induced testicular damage in rats. Testicular damage was induced in rats by injecting DOX (12.5 mg/kg, i.p., single dose) into rats. α-Bisabolol (25 mg/kg, i.p.) was administered to the rats along with DOX pre- and co-treatment daily for a period of 5 days. DOX-injected rats showed a decrease in absolute testicular weight and relative testicular weight ratio along with concomitant changes in the levels/expression levels of oxidative stress markers and Nrf2 expression levels in the testis. DOX injection also triggered the activation of NF-κB/MAPK signaling and increased levels/expression levels of pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β) and inflammatory mediators (iNOS and COX-2) in the testis. DOX triggered apoptosis, manifested by an increment in the expression levels of pro-apoptotic markers (Bax, Bcl2, cleaved caspase-3 and -9, and cytochrome-C) and a decline in the expression levels of anti-apoptotic markers (Bcl-xL and Bcl2) in the testis. Additionally, light microscopy revealed the changes in testicular architecture. α-Bisabolol rescued alterations in the testicular weight; restored all biochemical markers; modulated the expression levels of Nrf2-mediated antioxidant responses, NF-κB/MAPK signaling, endoplasmic reticulum (ER) stress, and apoptosis markers in DOX-injected testicular toxicity in rats. Based on our findings, it can be concluded that α-bisabolol has the potential to attenuate DOX-induced testicular injury by modifying NF-κB/MAPK signaling and the ER-stress-mediated mitochondrial pathway of apoptosis by invoking Nrf2-dependent antioxidant defense systems in rats. Based on the findings of the present study, α-bisabolol could be suggested for use as an agent or adjuvant with chemotherapeutic drugs to attenuate their deleterious effects of DOX on many organs including the testis. However, further regulatory toxicology and preclinical studies are necessary before making recommendations in clinical tests.

The impact of Nrf2/HO-1, caspase-3/Bax/Bcl2 and ATF6/IRE1/PERK/GRP78 signaling pathways in the ameliorative effects of morin against methotrexate-induced testicular toxicity in rats.

Methotrexate (MT) is a broadly used chemotherapeutic drug however its clinical use is confronted with several forms of toxicities containing testicular damage. The current study assessed the ameliorative effects of morin on MT-induced testicular damage with the investigation of its mechanism and the potential involvement of oxidative stress, inflammation, apoptosis and endoplasmic reticulum stress in such protection. The animals were divided into 5 distinct groups (7 rats in each group). Group 1 was control group, group 2 received MT-only (20mg/kg bw), group 3 received orally morin-only (100mg/kg bw), group 4 received MT (20mg/kg bw) + morin (50mg/kg bw) and group 5 received MT (20mg/kg bw) + morin (100mg/kg). In this study, morin was administered orally for 10 days, while MT was administered intraperitoneally on the 5th day. MT intoxication was linked with augmented MDA while decreased GSH levels, the enzyme activities of glutathione peroxidase, superoxide dismutase, and catalase and mRNA levels of HO-1 and Nrf2 in the testis tissues. MT injection caused inflammation in the testicular tissue via up-regulation of MAPK14, NFκB, TNF-α and IL-1β. MT application also caused apoptosis and endoplasmic reticulum stress in the testis tissue via increasing mRNA transcript levels of Bax, caspase-3, PERK, IRE1, ATF-6, GRP78 and down-regulation of Bcl-2. Treatment with morin at a dose of 50 and 100mg/kg considerably mitigated oxidative stress, inflammation, apoptosis and endoplasmic reticulum stress in the testicular tissue indicating that testicular damage related to MT toxicity could be modulated by morin administration.

Fluted pumpkin seeds protect the spermatogenesis score index and testicular histology of caffeine treated rats.

The present study was designed to evaluate the protective effect of fluted pumpkin seeds (FPS) against caffeine (CAFF) induced testicular toxicity in rats. Thirty young healthy male Wistar rats (196 ± 12 g) were randomly organized into five sets of six animals per each group: control, caffeine (CAFF; 50 mg kg-1 bw) and FPS co-treatment groups (CAFF + 50 mg FPS, CAFF + 100 mg FPS and CAFF + 200 mg FPS kg-1 bw). CAFF and FPS were administered daily and twice per week respectively by oral gavage for 40 days. CAFF treatment decreased testicular lactate dehydrogenase enzyme activity level, which was attenuated on co-administration with FPS at 50 and 100 mg kg-1 bw. Furthermore, CAFF decreased seminiferous epithelia thickness and spermatogenesis score index and increased the number of tubules with abnormal histological features, which were attenuated on co-administration with FPS at 50 mg kg-1 bw much more than at the higher doses (p < 0.05). CAFF did not affect malondialdehyde and glutathione concentrations and glutathione peroxidase (GSH-Px) activity in the testes whereas FPS co-treatment at the higher doses elevated glutathione level and GSH-Px activity and did not affect spermatogenesis score index at the highest dose (200 mg kg-1 bw). Testicular malondialdehyde concentrations remained unaffected in all FPS co-treatment groups. Overall, FPS is able to minimize the CAFF-induced testicular injury at lower than at the higher tested doses.

Fisetin ameliorates oxidative glutamate testicular toxicity in rats via central and peripheral mechanisms involving SIRT1 activation

ABSTRACT Objectives This study aimed to evaluate the potential mitigating effect of fisetin on monosodium glutamate (MSG)-induced testicular toxicity and investigate the possible involvement of silent mating type information regulation 2 homolog 1 (SIRT1) in this effect. Methods Forty male rats were divided into normal control, fisetin-treated, MSG-treated, and fisetin + MSG-treated groups. Testosterone, GnRH, FSH, and LH were measured in plasma, as well as SIRT1 and phosphorylated AMP-activated protein kinase (pAMPK) levels in testicular tissues using ELISA. Hydrogen peroxide (H2O2), nitric oxide (NO), and reduced glutathione (GSH) were measured colorimetrically, while Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) expression was relatively quantified using RT–PCR in testicular tissues. Results After 30 days, fisetin could ameliorate MSG-induced testicular toxicity by acting centrally on the hypothalamic-pituitary-gonadal axis, increasing plasma levels of GnRH, FSH, LH, and testosterone. Peripheral actions of fisetin on the testis were indicated as it increased testicular SIRT1 and pAMPK. Furthermore, it antagonized glutamate-induced oxidative stress by significantly lowering H2O2, NO, and relative NOX4 expression while significantly increasing reduced GSH levels. It also improved the architecture of the seminiferous tubules, reduced sperm abnormality, and increased sperm count. Discussion Fisetin ameliorates MSG-induced testicular toxicity via central and peripheral mechanisms making it a promising therapeutic target for male infertility.

Frankincense extract protects against testicular damage through augmentation of antioxidant defense mechanisms and modulation of apoptotic genes expression

Frankincense (Boswellia sacra Fluck.,) is traditionally used in the treatment of altered male fertile potential in several countries. This study evaluated the cytoprotective action of B. sacra oleo gum resin extract against cyclophosphamide (CP) induced testicular toxicity in rats (in-vivo) and lipopolysaccharide (LPS) induced cytotoxicity in human Leydig cells (in-vitro). The methanolic extract of B. sacra was standardized for the presence of different boswellic acids using high-performance liquid chromatography (HPLC) and volatile constituents in the extract were detected by gas chromatography–mass spectrometry (GC–MS). Two doses of B. sacra extract were used in the in-vivo study. The HPLC analysis showed that extract contains about 36% w/w of total boswellic acids and GC–MS analysis revealed the presence of another 71 different constituents. Administration of B. sacra extract to rats increased serum testosterone levels, antioxidant enzyme activities, and sperm count with improved sperm quality in a dose-dependent manner, when compared to CP treated animals. Boswellia sacra extract also protected the human Leydig cells against LPS-induced damage and increased the expression of the Bcl-2 gene along with a decrease in caspase-3 gene expression. The results of this study show that B. sacra extract has a protective effect on the male reproductive system.

The Synergetic Effect of Egyptian Portulaca oleracea L. (Purslane) and Cichorium intybus L. (Chicory) Extracts against Glucocorticoid-Induced Testicular Toxicity in Rats through Attenuation of Oxidative Reactions and Autophagy.

Long-term glucocorticoids can alter sperm motility, vitality, or morphology, disrupting male reproductive function. This study scrutinized the synergistic benefits of two Egyptian plants against dexamethasone (Dexa)-induced testicular and autophagy dysfunction in male rats. Phytochemical ingredients and the combination index were estimated for Purslane ethanolic extract (PEE) and Chicory water extract (CWE). Four control groups received saline and 100 mg/kg of each PEE, CWE, and PEE/CWE, daily for 8 weeks. Dexa (1 mg/kg daily for 6 weeks) induced infertility where PEE, CWE, and PEE/CWE were given. Seminal analysis, male hormones, glycemic and oxidative stress markers, endoplasmic reticulum (ER) stress markers (Sigma 1R and GRP78), and autophagy regulators (Phospho-mTOR, LC3I/II, PI3KC3, and Beclin-1, P62, ATG5, and ATG7) were measured. The in vitro study illustrated the synergistic (CI < 1) antioxidant capacity of the PEE/CWE combination. Dexa exerts testicular damage by inducing oxidative reactions, a marked reduction in serum testosterone, TSH and LH levels, insulin resistance, ER stress, and autophagy. In contrast, the PEE and CWE extracts improve fertility hormones, sperm motility, and testicular histological alterations through attenuating oxidative stress and autophagy, with a synergistic effect upon combination. In conclusion, the administration of PEE/CWE has promised ameliorative impacts on male infertility and can delay disease progression.

Ephedra herb reduces adriamycin-induced testicular toxicity by upregulating the gonadotropin-releasing hormone signalling pathway.

We investigated the protective effects of ephedra herb (HEPH) on adriamycin-induced testicular toxicity in rats and explored the potential mechanisms underlying these effects. A rat model of adriamycin injury was established, and sperm motility-related indicator and oxidative stress levels in the testis were evaluated. Serum levels of sex hormones and levels of testicular cell apoptosis were detected by enzyme-linked immunosorbent assay and flow cytometry, respectively. Western blotting (WB), immunofluorescence analyses, and reverse transcription-polymerase chain reaction (RT-PCR) were performed to evaluate the gonadotropin-releasing hormone (GnRH) signalling pathway- and meiosis-related genes and proteins. In subsequent in vitro experiments, adriamycin was used to stimulate GC-1 cells, which were treated with HEPH, ephedrine, or pseudoephedrine. Cell viability was assessed using flow cytometry to detect apoptosis and reactive oxygen species, whereas the GnRH signalling pathway and levels of meiosis-related genes and proteins were evaluated by InCell WB, a high-content imaging system, and RT-PCR. Per in vivo experiments, HEPH restored testicular weight and function, sperm characteristics, serum and tissue hormonal levels, and antioxidant defences and significantly activated the GnRH signalling pathway- and meiosis-related protein levels. All protective effects of HEPH against adriamycin-induced injury were antagonised by the GnRH antagonist cetrorelix. In vitro, HEPH, ephedrine, and pseudoephedrine significantly reduced adriamycin-induced GC-1 cell apoptosis and reactive oxygen species levels and increased the expression of GnRH signalling pathway- and meiosis-related proteins. The effect of pseudoephedrine was greater than that of ephedrine, and these findings may be an important basis for understanding the effects of HEPH.

Arrested Acetylene-Induced Pulmonary and Testicular Toxicity in Rats Through Treatment With Polyphenols

Occupational exposure to potentially harmful substances is one of the dangers associated with industrial jobs. This study evaluated the modulatory influence of selected dietary polyphenols on the pulmonotoxic and testiculotoxic effects of crude acetylene, an industrial gas used in welding metals. Wistar rats were exposed to 58 000 ppm acetylene, 20 min daily for 30 days, in a 36 L glass inhalation chamber. Some acetylene-exposed animals were treated concurrently with 30 mg/kg quercetin, rutin, caffeic acid, ferulic acid, or coumaric acid. At the end of the treatment sessions, the levels of superoxide dismutase, reduced glutathione, glutathione peroxidase, lactate dehydrogenase, and hormonal markers in rats exposed to acetylene were significantly decreased, with a concomitant increase in lipid peroxidation, nitric oxide level, cholesterol concentration, and histopathological abnormalities. These damaging biochemical and histopathological changes were significantly ameliorated in animals administered the polyphenols. Quercetin showed greater ameliorative activity than rutin while the phenolic acids exhibited increasing levels of ameliorative activity in the order: caffeic acid > ferulic acid > coumaric acid. These results indicate that inhalation of crude acetylene is deleterious to the lungs and testes, and polyphenols provide protection against these detrimental effects.

Maternal supplementation of \u03b1-lipoic acid attenuates prenatal cytarabine exposure-induced oxidative stress, steroidogenesis suppression and testicular damage in F1 male rat fetus

BackgroundCytarabine (Ara-C) is an anticancer drug, which is considered as the mainstay in the treatment of hematological malignancies, known to cause various teratogenic effects. Alpha-lipoic acid (ALA) is a natural antioxidant and its supplementation proved to improve pregnancy outcomes in several pathological conditions. We aimed at exploring the benefits of maternal supplementation of ALA against in-utero Ara-C exposure-induced testicular toxicity in rat fetuses.MethodsPregnant rats (dams) received normal saline (control group), ALA 200 mg/kg (ALA group), Ara-C 12.5 mg/kg (Ara-C 12.5 group), Ara-C 25 mg/kg (Ara-C 25 group), and Ara-C 25 mg/kg + ALA 200 mg/kg (protection group) from gestational day (GD)8 to GD21. Ara-C and ALA were administered via the intraperitoneal and oral routes, respectively. The day of parturition was considered as postnatal day (PND)1. On PND1, all the live male pups were collected. The maternal parameters evaluated include (a) food intake, (b) bodyweight, and (c) oxidative stress (OS) markers. The fetal parameters evaluated include (a) bodyweight, (b) anogenital distances (AGD), (c) testicular weight (d) testicular testosterone levels (e) testicular histopathology, and (f) morphometrical parameters.ResultsA significant and dose-dependent decrease in maternal food intake, weight gain, and an increase in oxidative stress (OS) were observed in the pregnant rats of the Ara-C groups as compared to pregnant rats of the control group. Further, a significant and dose-dependent (a) reduction in bodyweight, AGD, testicular weight, and testosterone levels, (b) increase in OS, and (c) structural and morphometrical anomalies in fetal testes were observed in fetuses of Ara-C groups as compared to fetuses of the control rats. These deleterious effects observed in the Ara-C groups were found to be diminished in the pregnant rats and fetuses of the Protection group as compared to the pregnant rats and fetuses of the Ara-C 25 group.ConclusionsFrom the results of this study, we conclude that the maternal supplementation of ALA may ameliorate the Ara-C exposure-induced impairment in prenatal development and function of the testes in the rat fetuses. However, future experimental and clinical studies are warranted to explore the possible mechanisms involved in the protection offered by maternal supplementation of ALA against Ara-C induced testicular toxicity.Graphical

Curcumin improves the protective effects of quercetin against atrazine-induced testicular injury in adult Wistar rats.

This study evaluated the beneficial protective effect of cotreatment of curcumin (CUR) and quercetin (QUE) on atrazine (ATZ)-induced testicular toxicity in rats. ATZ challenge diminished luteinizing hormone, follicular stimulating hormone, testosterone and myeloperoxidase enzyme activity, but these effects were attenuated on co-treatment with CUR and QUE. Also, co-treatment of CUR + QUE was better than separate administration of QUE at diminishing malondialdehyde and glutathione and improving tumour necrosis factor-α concentration, germ cell numbers (spermatogonia, spermatocytes and round spermatids) and epididymal sperm quality. Histologically, smaller sized tubules with degenerated epithelia and few germ cells were seen in the seminiferous tubules of the ATZ group whereas CUR + QUE pretreatment improved the histo-morphologic features of the tubules compared to the ATZ group and was also better than separate administration of QUE. We conclude that CUR can improve the protective effects of QUE against ATZ-induced testicular injury by enhancing the levels of reproductive hormones, recovering testicular biochemical parameters and improving the histological features of the testes.

Antioxidant Effects of Ethanolic Extract of Piper guineense (Uziza) Leaves on Lead-Induced Testicular Toxicity in Wistar Rats

Piper guineense (uziza) leaves may have therapeutic input on male infertility caused by Lead exposure. This study investigated the antioxidant activities of the ethanolic extract of Piper guineense leaves (EEPL) on lead-induced testicular toxicity in rats. Twenty male wistar rats (150-200g) were divided into 4 groups consisting of 5 rats each. Control received 1ml of distilled water, lead only received 150mg/kg of lead, low dose received 150mg/kg of lead + 300mg/kg of EEPL, high dose received 150mg/kg of lead + 600mg/kg of EEPL. Administration was done orally for 14 days and then sacrificed. Blood was collected and analysed for serum testosterone and testes were harvested and homogenised for testicular antioxidant enzymes and zinc levels. Data was analysed for ANOVA using Graph Pad Prism 5. Lead exposure negatively affected the antioxidant enzymes, testosterone and zinc levels. Administration of EEPL significantly (p&lt;0.05) increased the testosterone and zinc levels in a dose dependent manner. EEPL also significantly (p&lt;0.05) increased the testicular Superoxide dismutase, Catalase, and Glutathione peroxidase levels and significantly decreased the testicular Malondialdehyde levels. Piper guineense leaves ameliorate testicular oxidative stress damage induced by lead toxicity.

Tiliacora triandra attenuates cisplatin triggered hepatorenal and testicular toxicity in rats by modulating oxidative inflammation, apoptosis and endocrine deficit.

Cisplatin (CIS) is a platinum based anticancer drug that has demonstrated significant efficacy against various types of cancers. Unfortunately, this drug is also famous for its severe side effects on delicate organs. Herein this study examined the hepatorenal and testicular protective effects of TiTE against CIS-induced hepatorenal and testicular insults. Rats were administered with TiTE (250 and 500 mg/kg body weight) for 4 weeks, while a single dose of CIS (2.5 mg/kg body weight) was injected once per week from week 2 to week 4. Treatment with TITE significantly attenuated CIS-induced increases in serum creatinine, blood urea nitrogen (BUN), uric acid, alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Furthermore, TiTE treatment also decreased oxidative stress (MDA) inflammations (TNF-α, IL-1β, IL-6, NF-κB) and apoptosis (caspase-3 activity) and restored hepatorenal and testicular antioxidant defense (SOD, CAT and GPx) in CIS treated rats. Additionally, the TiTE improved sperm count, motility and viability, and ameliorated the reduced serum levels of testosterone, follicle stimulating hormone (FSH) and luteinizing hormone (LH) in CIS-injected rats. TiTE also curtailed hepatorenal and testicular histological changes in CIS treated rats. The findings from the study indicated that TiTE displayed hepatorenal and testicular protective effects via inhibition of oxidative stress-mediated inflammation and endocrine imbalance in rats.

Protective effects of Nigella sativa oil against bisphenol A-induced testicular toxicity in rats

The study investigated the protective effect of Nigella sativa (NS) oil against testicular damage induced by bisphenol A (BPA). A total of 36 Wistar Albino rats were divided into 4 groups: control (1ml olive oil), NS (5 ml/kg NS), BPA (100 mg/kg BPA in 1 ml olive oil), BPA+NS (100 mg/kg BPA + 5 ml/kg NS). During the 30-day experiment, all substances were administered by oral gavage. The levels of testosterone and LH in serum, as well as MDA, GSH, SOD, TNF-α, IL-6 and IL-10 levels in testicular tissue were measured by ELISA. Spermatological examinations and histopathological analyses of testicular tissue were also performed. BPA was found to raise LH while reducing the serum testosterone level. BPA caused a decrease in GSH, SOD, TNF-α and IL-6, but an increase in MDA and IL-10. BPA also reduced sperm motility, plasma membrane integrity, mitochondrial activity and acrosome membrane integrity. Oedema, hyperaemia, mononuclear cell infiltration in the interstitial tissue, as well as giant cell formations, degeneration and necrosis in the seminiferous tubules were seen in the BPA group. In addition, reductions in germinative epithelium, tubule diameter and the Johnson testicular score were noted. In rats receiving NS, hormonal profile, oxidative stress markers and cytokine levels were within normal limits. NS improved sperm motility, mitochondrial activity (JC1), plasma membrane integrity (SYBR-14) and partially acrosome membrane integrity (FITC-PNA). NS reduced testis inflammation, significantly ameliorated the testicular score and, to a lesser extent, increased germinative epithelium thickness and tubule diameter. It was concluded that NS has a protective effect against BPA-induced testicular toxicity.

The ameliorative effects of Alpinia officinarum rhizome hydroalcoholic extract on cisplatin-induced testicular toxicity in rats.

In this study we evaluated the influence of Alpinia officinarum rhizome extract (AO) on the alleviation of testicular damage induced by cisplatin in rats. The study groups included the control group, AO-administered group, cisplatin-administered group, and three groups administered with cisplatin and AO (different concentrations of 100, 200, and 400 mg/kg). On the 14th day we removed the testes of the rats, and the testicular organ parameters were measured. Moreover, through the malondialdehyde concentration we assessed the oxidative stress and superoxide dismutase (SOD) activity of the testes and ran a histopathological analysis. The results demonstrated that cisplatin-induced oxidative stress and severe testicular damage on the AO-administered group showed no harm compared with the control group. AO- treatment in cisplatin-received rats led to the reduction of oxidative stress, enhancement of SOD activity, and prevention of testicular damage. The lowest testis damage was attributed to the group which received 400 mg/kg of AO compared to 100 and 200 mg/kg. Overall, the Cis+/AO+400 group had the best antioxidant effect. The findings could lead to changes in cancer care guidelines that incorporate phytochemicals, making cancer therapies safer.

Glutamine Supplementation Attenuates Bisphenol A-Induced Testicular Toxicity in Rats.

The induction of testicular toxicity by bisphenol A (BPA) may involve oxidative stress. Glutamine (Gln) is a rate limiter for the synthesis of glutathione (GSH), which inhibits oxidative stress. This study assessed the potential of BPA to preserve testicular structure and function in BPA-treated albino rats. Thirty-two adult male albino rats (210-250 g) were randomly allocated to 4 (A-D) of 8 rats per group with the approval of the Research Ethics Committee. Groups B-D were orally treated with Gln (20 mg/kg body weight), BPA (50 mg/kg body weight) and Gln (20 mg/kg body weight) + BPA (50 mg/kg body weight) daily for 65 days, respectively. Group A (control) was orally treated with normal saline (0.2 mL) daily for 65 days. At the termination of treatment, the rats were weighed and anaesthetized blood samples were collected and evaluated for gonadal hormones. The testes were weighed and evaluated for sperm parameters, oxidative stress markers and histology. The data were analysed using one-way analysis of variance and Bonferroni post hoc test. BPA caused a significant (P < 0.001) decrease in testis and body weights, sperm count, volume, motility and normal morphology when compared to the control. BPA significantly (P < 0.001) decreased serum testosterone, follicle-stimulating hormone, luteinising hormone, testicular catalase, superoxide dismutase, GSH and GSH peroxidase levels relative to control. Significantly (P < 0.001) increased serum prolactin, estradiol and testicular malondialdehyde levels occurred in BPA-treated rats relative to control. The testes of BPA-treated rats showed sloughing and coalescence of germ cells. However, Gln supplementation prevents BPA-induced testicular toxicity. Gln supplementation restored testis histology. Based on the observation in this study, Gln seems effective against BPA-induced testicular toxicity.

Sildenafil aggravates adriamycin-induced testicular toxicity in rats; a preliminary investigation

Male reproductive toxicity is a well-established side effect of the chemotherapeutic drug adriamycin (ADR). Sildenafil (SIL) is a phosphodiesterase inhibitor known to enhance the chemosensitivity of cancer cells to ADR. However, there is a scarcity of information on the effect of SIL on ADR-induced testicular toxicity. In this study, SIL (5, 10, or 20 mg/kg/day) was administered to male rats for 7 days, followed by a single intraperitoneal injection of ADR (20 mg/kg) on day 7. Control rats received either ADR, SIL, or normal saline for 7 days. Epididymal sperm were collected from the testes to assess the effects on sperm quality, quantity, and serum testosterone concentration was also determined. ADR treatment caused a decrease in sperm motility and elevated the percentage of sperms with tail defects which worsened in combination with SIL (20 mg/kg). Furthermore, ADR alone or in combination with SIL dose-dependently increased total sperm abnormalities. SIL (20 mg/kg) plus ADR also decreased sperm count and lowered testosterone level compared to ADR-only rats. In conclusion, exposure of rats to SIL before ADR treatment has the potential to worsen ADR-induced testicular toxicity.

Investigation of the effects of hesperidin administration on abamectin-induced testicular toxicity in rats through oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, autophagy, and JAK2/STAT3 pathways.

In this study, the potential effects of hesperidin (HES) on chronic toxicity caused by abamectin (ABM) in the testicular tissue were investigated through oxidative stress, inflammation, endoplasmic reticulum stress (ERS), apoptosis, and autophagy pathways. Male Sprague Dawley rats were used in the study. Animals in the ABM group were orally administered 1 mg/kg ABM every other day for 28 days, while HES used against ABM was given at 100 or 200 mg/kg 30 min after ABM administration for 28 days. Markers of oxidative stress, inflammation, ERS, apoptosis, and autophagy in the testicular tissues removed after the animals are sacrificed were analyzed using biochemical, real-time polymerase chain reaction (RT-PCR), or western blot techniques. The results obtained showed that ABM caused oxidative stress, and triggered ERS, inflammation, apoptosis, and autophagy. On the other hand, HES showed antioxidant effect by increasing superoxide dismutase, catalase, glutathione peroxidase enzyme activities, and glutathione levels in testis tissue and attenuated lipid peroxidation. Accordingly, MAPK14 reduced the NF-κB, IL-1β, TNF-α, and IL-6 expression levels, presenting an anti-inflammatory effect. In addition, Bax protected against apoptosis and autophagy by reducing the caspase-3, beclin-1, LC3A, and LC3B expressions, and increasing Bcl-2 expression. It was observed that HES also interrupted the JAK2/STAT3 signaling pathway by suppressing IL-6 expression. Taken into consideration together, HES provided significant protection against the destruction caused by ABM in testicular tissue with antioxidant, anti-inflammatory, antiapoptotic, and anti-autophagic effects. Thus, it was revealed that HES has the potential to serve as an alternative treatment option in ABM toxicity.

Effects of Virgin coconut oil on Testicular toxicity induced by Cadmium in rats

One of major threat to the environmental pollution is the contamination the by various heavy metals. Cadmium is found to have toxic effects on testis. VCO is increasingly getting the reputation of being the most versatile and healthiest antioxidant. Objective: To study the effect pre-treatment of virgin coconut oil in cadmium induced testicular toxicity in rats. Materials and methods: Institutional ethics committee clearance was obtained before beginning the experiments. Male rats of wistar strain approximately 150-200 gm body weight was used. They were housed in the central animal house under controlled conditions of temperature and light with normal rat feed and drinking water. Animals were divided into four groups with 6 rats in each group. Sperm count and sperm morphology was done. One of the testis was used for histopathological study. The data was expressed as mean  SD. Significance of the test was set at p&lt;0.05. Results: In the present study administration of cadmium chloride showed a significant decrease in the testicular and epididymal weight as well as sperm count and testosterone level and increase in sperm shape abnormality. Pre-treatment with Virgin coconut oil showed a significant increase in the testicular and epidydimal weight as well as sperm count and testosterone level and decrease in sperm shape abnormality Testicular section in normal control rats and Virgin treated rats showed normal features. But, in cadmium treated rats the testis showed necrosis of most of the tubules but rats pre-treated with virgin coconut oil showed that less than 25 % of the tubules had necrosis. Conclusion: In conclusion, present study showed that Cadmium administration showed a damaging effect on the testis and Virgin coconut oil showed protective role in attuning cadmium induced testicular damage

The protective effect of crocin on cisplatin-induced testicular impairment in rats

BackgroundSide effects of cisplatin (CIS) such as testicular toxicity restrict its clinical use. Instead, evidence indicates that crocin (CR) has synergistic anti-cancer potential with CIS and exhibited beneficial effects on CIS-induced hepatorenal damage. The aim of this study was to investigate the protective potential of CR against CIS-induced testicular toxicity in rats.MethodsFifty adult male Wistar rats randomly assigned to five equal groups including control, CIS, and CIS plus CR at doses of 6.25 mg/kg (CIS + CR6.25), 25 mg/kg (CIS + CR25), and 100 mg/kg (CIS + CR100). CIS and CIS + CR groups received a single intraperitoneally (i.p.) injection of CIS (7 mg/kg). CR (6.25–100 mg/kg i.p.) injections were started three days before the CIS injection and continued once a day for up to 13 days. On the 14th day, all animals were sacrificed and their blood samples and testes were removed for biochemical and histological analyses.ResultsCompared to the control group, CIS significantly decreased relative testis weight (0.28 vs. 0.39, p < 0.001), testosterone level (0.3 vs. 2.31 ng/mL, p < 0.001), germinal layer area (25,886 vs. 35,320 µm2, p < 0.001), superoxide dismutase (SOD) (0.9 vs.1.73 U/mg, p < 0.001) and increased testicular lipid peroxidation (3.05 vs. 15.35 nmol/mg, p < 0.001). CR at 25 mg/kg ameliorated testicular lipid peroxidation and enhanced SOD activity compared to CIS group (p < 0.05). Besides, CR treatment at the maximum dose (100 mg/kg) resulted in reversing CIS effects on testis weight, testosterone level, SOD, lipid peroxidation, and germinal layer area.ConclusionsThese findings demonstrated that CR co-treatment could prevent CIS-induced testicular toxicity in rats.