Rat Testicular Tissue Research Articles

Combined Effects of Chrysin Supplementation and Exercise Training on Diabetes-Induced Oxidative Stress and Apoptosis in Rat Testicular Tissue.

Diabetes mellitus (DM), one of the most pervasive and enduring metabolic diseases, has been demonstrated to adversely impact male fertility. Conversely, both exercise training and Chrysin have been identified as potential interventions capable of mitigating the deleterious effects of diabetes on spermatogenesis. Thus, the current study aims to explore the individual and combined influences of Chrysin supplementation and running exercise on oxidative stress and germ cell apoptosis in the testicular tissue of diabetic adult rats. In this experimental study, the DM was induced by streptozotocin (STZ,50 mg/kg). Rats were divided into control (received STZ solvent), DM-sole, Chrysin-sole (50 mg/kg, daily), moderate-intensity running exercise training (MIRET-sole, warm-up, 5 minutes at 30% of Smax1 (Maximum speed); Moderate intensity exercise, 60 minutes at 60% of Smax1, and recovery, 5 minutes to 30% of Smax1), DM+Chrysin, DM+MIRET, and DM+MIRET+Chrysin. Following 8 weeks, the histopathological changes (Johnson's score, epithelial height, and tubular diameter), testicular malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX), and the mRNA levels of anti-apoptotic gene Bcl-2 and pro-apoptotic gene Bax was analyzed. Chrysin solely and simultaneous with MIRET could remarkably (P=0.001) improve the DM-induced histopathological damages, increase the testicular SOD and GPx levels, and decline the DM-increased MDA content. Moreover, our results showed that Chrysin solely and more simultaneously with MIRET could significantly (P=0.001) decrease the mRNA expression of Bax and improve the Bcl-2 expression and rebalance the Bax/Bcl-2 balance. Our findings showed that co-administration of Chrysin along with MIRET can significantly ameliorate the DM-induced histopathological, and biochemical impairments and reduce the pro-apoptotic impact of DM on testicular tissue.

Investigation of the effects of diisobutyl phthalate on rat testicular tissue: a histopathological and morphometric evaluation

Phthalates are a group of chemicals used to make plastics more durable, and they are often called plasticisers. Additionally, these chemicals are found in hundreds of products such as floor coverings, lubricating oils, and personal care products (soaps, shampoos, hair sprays). Consumer products containing phthalates can result in human exposure through direct contact and use, indirectly through leaching into the other products or general environmental contamination. In this study, the effects of Diisobutyl phthalate a commonly used phthalate, were investigated histopathologically and morphometrically to determine whether it is one of the causes of increased infertility in recent years. Two study groups of albino Wistar albino rats (total n: 40) were formed; the control group (untreated control group, solvent-corn oil the control group) and the experimental group. DiBP was administered by oral gavage to the experimental group in 3 different doses (0.25–0.5–1 mL/kg/day) mixed with corn oil every day for 28 days. At the end of the experiment, testicular tissue samples taken from all the experimental and control animals were evaluated histopathologically and morphometrically by light microscopy after routine preparation. Degeneration/atrophic tubules were quite prominent in the sections. Tubules containing degenerated germ cells and tubules devoid of germ cells were observed. It was determined that in most tubules, only tubules covered with Sertoli cells remained due to germ cell death. In addition, multinucleated giant cells were frequently encountered in such tubules. Dilatation and thickening in the basal lamina of the seminiferous tubule were accompanied by decreased PAS-positive reaction. The morphometric results supported the histopathological findings. Significant dose-related morphometrical changes (p<0.0001), including seminiferous tubule diameter, tubular lumen diameter, spermatogenic cell line height and basal lamina thickness were observed between the control and administration groups. According to the control, sham and G1, the number of these multinucleated cells (MGC) increased in G2 and G3 but these increases were statistically insignificant (p > 0.9999). In conclusion, it was observed that irreversible damage occurred in the testicular tissues of DiBP-exposed groups, and it was decided that this could be the cause of infertility. Therefore, we recommend the use of an alternative plasticiser with proven reliability.

Alterations Expression of Key RNA Methylation (m6A) Enzymes in Testicular Tissue of Rats with Induced Varicocele.

Epigenetics impacts male fertility and reproductive disorders. RNA modifications, like m6A, influence RNA metabolism. Varicocele contributes to male infertility, and oxidative stress affects sperm function. This study investigates the expression of key RNA modification enzymes in a rat varicocele model, aiming to elucidate the relationship between varicocele, oxidative stress, and fertility. Fifteen male Wistar rats were divided into Control, Sham, and Varicocele induction groups. Varicocele was induced in the rats surgically. After 8 weeks, testicular tissues and sperm were collected for analysis, including histopathological assessment and evaluation of sperm parameters, functional tests, and gene expression of key RNA modification enzymes: METTL3 as a writer, ALKBH5 and FTO as erasers, and YTHDF2 as a reader involved in recognizing m6A-modified RNA using qRT-PCR. One-way ANOVAwithpost-hoc Tukey HSDwas used forcomparing tests within groups. Varicocele induction resulted in histological changes in testicular tissues, including irregularly variable-sized seminiferous tubules. Sperm parameters were significantly affected, with lower concentration, motility, and higher percentage of abnormal sperm in the varicocele group. Increased levels of oxidative stress markers (Sperm lipid peroxidation, and intracytoplasmic ROS) and sperm DNA damage were observed, indicating the presence of oxidative stress in varicocele. Moreover, the expression of key enzymes involved in RNA metabolism was downregulated in the varicocele group. These findings highlight the detrimental impact of varicocele on testicular health, sperm quality, and gene expression, providing insights into the underlying mechanisms of male infertility associated with varicocele.

Effects of sitagliptin and L-theanine combination therapy on testicular tissue in rats with experimental diabetes

This study examines the impact of the combination of sitagliptin and L-theanine on the testis tissue of rats with experimental diabetes. Diabetes mellitus, a chronic metabolic illness, significantly reduces quality of life and can cause male infertility by decreasing sperm count, motility, and testosterone levels. Rats were allocated to five separate groups: control, diabetes, L-theanine, sitagliptin, and combination therapy. The measurements encompassed blood glucose levels, body weight, serum insulin levels, and the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR). The histological examination of testicular tissue was conducted using H&E, PASH, caspase-12, and PCNA staining techniques, in addition to a TUNEL assay to detect apoptosis. Levels of oxidative stress indicators, including glutathione peroxidase (GPX), malondialdehyde (MDA), and catalase, were also evaluated. The results showed that the group of individuals with diabetes had significantly higher levels of blood glucose, apoptotic indices, GPX, catalase, and MDA levels and activities in comparison with the control group. Although both the L-theanine and sitagliptin groups exhibited some improvement, the combination therapy demonstrated the most significant decrease in histopathological damage and apoptotic markers. These results indicate that the combination of sitagliptin and L-theanine may significantly decrease testicular damage caused by diabetes, making it a promising therapeutic strategy.

Effects of Methionine Chronic Administration on Testicular Tissue in Rats: A Histopathological and Immunohistochemical Study

Effects of Methionine Chronic Administration on Testicular Tissue in Rats: A Histopathological and Immunohistochemical Study

Sulforaphane substantially impedes testicular ferroptosis in adult rats exposed to di-2-ethylhexyl phthalate through activation of NRF-2/SLC7A11/GPX-4 trajectory.

Di-2-ethylhexyl phthalate (DEHP) is a common plasticizer with a deleterious impact on testicular functionality and male fertility. Growing evidence implicates ferroptosis as one of the plausible mechanisms for DEHP-induced testicular injury. Sulforaphane (SFN) is a natural isothiocyanate displaying beneficial effects on testicular injury in several animal models. Herein, we explored the potential protective effect of SFN on testicular ferroptosis and toxicity evoked by DEHP. Adult male Wistar rats were equally distributed into three groups (n = 6/group): (i) CON group; (ii) DEHP group, received DEHP (2g/kg PO) for 4weeks; and (iii) DEHP + SFN group, received SFN (10mg/kg, PO) 1week prior to DEHP then concurrently with DEHP for further 4weeks. Compared to CON group, exposure to DEHP caused testicular atrophy, deteriorated testicular architecture, testicular fibrosis, reduced sperm count and motility, higher sperm deformity, and declined serum testosterone level. All these abnormalities were ameliorated by SFN preconditioning. Additionally, pretreatment with SFN reversed the increased aromatase level and upregulated the steroidogenic markers in testes of DEHP-exposed rats. SFN pretreatment also counteracted DEHP-induced oxidative stress and boosted the total antioxidant capacity in testicular tissue via activation of the nuclear factor erythroid 2-related factor 2 (NRF-2) and its downstream target, hemeoxygenase-1 (HO-1). Moreover, SFN preconditioning mitigated DEHP-induced ferroptosis through up-surging SLC7A11, GPX-4, and GSH, while suppressing iron overload and ACSL4-induced lipid peroxidation in testicular tissue of rats. These findings may nominate SFN as a promising protective intervention to alleviate testicular ferroptosis associated with DEHP exposure through activation of NRF-2/SLC7A11/GPX-4 trajectory.

Study of Histological Changes of Testis in Rats of Different Ages When Exposed to Frequency 10GHZ Within The X-Band Microwave

This study investigates the impact of 10 GHz microwave exposure, within the X-band range, on rat testicular tissue and sperm development across different age groups. Laboratory rats were divided into a control group of six, which was not exposed to microwaves, and a treatment group of 18, further split into three age-based subgroups (8–12 weeks, 12–16 weeks, and 16–20 weeks), each containing six rats exposed to 10 GHz microwaves for 2.5 hours daily over five weeks. The findings revealed no histological changes in the control group. However, in the treated groups, significant alterations were observed: the youngest group showed a lack of sperm formation and loss of spermatocytes; the middle group displayed malformed sperm and reduced numbers; and the oldest group experienced a decrease in sperm count and minor shape alterations. Additionally, after five weeks, all treated groups exhibited damage to the testicular interstitial tissue, including ruptures and space formation between seminiferous tubules. This study suggests potential risks of microwave exposure on reproductive health and lays the groundwork for future research in this area.

Potential Protective Effect of Hesperidin (Vitamin P) against Glyphosate-Induced Spermatogenesis Damage in Male Rats: Biochemical and Histopathological Findings on Reproductive Parameters.

The aim of this study was to investigate the effectiveness of hesperidin (HES) on testicular histopathological changes, biochemical changes, and semen characteristics in rats exposed to glyphosate (GLP). The control group was given a normal diet devoid of GLP and HES, the HES group was given 100 mg/kg/day HES with the normal diet, the GLP group was given GLP at the LD50/10 dose of normal feed, which was 787.85 mg/kg/day, and the GLP + HES group was given normal feed containing 787.85 mg/kg/day LD50/10 dose of GLP in addition to 100 mg/kg/day HES. GLP administration reduced sperm motility, sperm plasma membrane integrity, glutathione levels, and total antioxidant levels in the testicular tissues of rats. Moreover, it caused an increase in right testis and left epididymis weights, abnormal sperm counts, malondialdehyde levels, total oxidant status, and DNA damage. The HES treatment showed curative effects on these parameters. Furthermore, HES was effective in lessening the histopathological damage that was caused by GLP. The results showedthat HES protects spermatological parameters and DNA integrity, improves antioxidant defenses, and lowers the damage and lipid peroxidation caused by GLP in testicular tissue.

The effects of testicular stromal stem cells on surgically injured testicular tissue in rats.

This study investigated the effects of transplanted testicular stromal stem cells (tSSCs) on surgically damaged testis tissue. Ten-week-old male Wistar albino rats were divided into three groups: control (n = 6), damage (DG) (n = 6) and testicular stromal stem cell (TSSC) (n = 6) groups. Surgically induced damage was inflicted on the left testes of both the DG and TSSC groups, with no intervention on the right testes. In the TSSC group, damaged testes were treated with transplanted tSSCs, followed by orchiectomy after 15 days. Testes tissues were stained with haematoxylin-eosin (H&E), and recovery rates of functional structures were assessed by modified Johnsen scoring. The effects of tSSCs on testicular tissue were demonstrated by immunohistochemistry using BAX, BCL-2 and caspase 3. Serum testosterone levels were analysed using the enzyme-linked immunosorbent assay (ELISA) method. Surgical damage caused germ cell degeneration in some seminiferous tubules and a decrease in interstitial areas. With tSSC treatment, improvements in testicular architecture were identified through spermatogenesis in the seminiferous tubules and normal histological structures in the interstitial areas. Correspondingly, in the modified Johnsen score, the DG group showed a significant difference compared to the other groups (p = 0.001). High expressions of BAX, BCL-2 and caspase-3 in the DG group revealed prominent features of apoptosis. With the injection of tSSCs, these expressions significantly normalized according to H score analysis (all p = 0.004). Although serum testosterone levels in the tSSC group were higher compared to the control and DG groups, this difference was not statistically significant (p = 0.119). This study suggests transplanting tSSCs could accelerate tissue healing after testicular sperm extraction (TESE) surgery for azoospermia patients, potentially paving the way for a new and important clinical treatment.

Ameliorative effects of sinapic acid against vancomycin-induced testicular oxidative damage, apoptosis, inflammation, testicular histopathologic disorders and decreased epididymal sperm quality

In this study, it was aimed to determine the effect of sinapic acid (SNP), a polyphenol with antioxidant, anti-inflammatory and antibacterial properties, on testicular damage caused by vancomycin (VCM), a widely used antibiotic against gram positive bacteria. A total of 35 male Sprague Dawley rats were used in the study, divided into five groups: control, VCM, SNP, VCM + SNP 10, and VCM + SNP 20. Following a week of oral administration, the rats were euthanized under sevoflurane anesthesia. While the VCM group had a significant increase in MDA levels, the SNP administration inhibited the increase in MDA levels. VCM led to a significant decrease in GSH levels, SOD, CAT, and GPx activity in the testicular tissue of rats, while SNP administration increased these antioxidant levels. SNP administration decreased the mRNA expression levels of VCM induced Nrf-2, HO-1, and NQO1 in testicular tissue while increasing the levels of MAPK14, MAPK15, JNK, P53, Apaf-1, Caspase-3, Caspase-6, Caspase-9, and Beclin-1 mRNA transcript levels. The VCM group showed a significant increase in Bax and NF-κB levels in testicular tissue, while Bcl-2 levels decreased. VCM significantly decreased sperm motility and increased the percentage of damaged sperm in rats. Histopathological results revealed that VCM caused disruption of basement membranes and disorganization of seminiferous tubules, but SNP administration preserved testicular histology. As a result, VCM increased oxidative stress, apoptosis, and autophagy in the testicular tissue of rats, altered testicular histopathology, and decreased sperm quality, while SNP decreased these effects.

Effect of hepatic ischemia reperfusion on testicular tissue in rats

Effect of hepatic ischemia reperfusion on testicular tissue in rats

Ameliorative potentials of diosmin and hesperidin fractions on chlorpyriphos-induced changes in reproductive hormones, sperm characteristics, and testicular glycogen in male Wistar rats.

Reproductive deficiency is a major outcome of pesticide exposure sequel to cellular oxidative damage to sex organs. Flavonoid possess potent antioxidant capacities to mitigate pesticide related cellular injury. The present investigation examined the mitigative effect of micronized purified fractions of diosmin and hesperidin on reproductive hormones, sperm parameters, and testicular glycogen in male Wistar rats after sub-chronic Chlorpyriphos (CPF) exposure. Twenty-five male Wistar rats (120-145g) were randomly allocated five rats per group. Group I (DW) received distilled water (2ml/kg), Group II (S/oil) received soya oil (2ml/kg), Group III (DAF) received Daflon at 1000mg/kg, Group IV (CPF) received Chlorpyriphos (7.74mg/kg), and Group V (DAF + CPF) received Daflon (1000mg/kg) followed by CPF (7.74mg/kg) after 30min of Daflon. This regimen was administered daily for 60days. After cervical venesection under light chloroform anesthesia, blood samples were examined for levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone. Each rat's testicular tissue was quickly cut, collected, and glycogen evaluated. Sperm concentration, motility, morphology, and viability were measured in the right caudal epididymis. Results revealed that the untreated CPF group had significantly lower FSH, LH, testosterone, testicular glycogen, and sperm concentration. Additionally, CPF group sperm characteristics were abnormal compared to other groups. These reproductive hormones, testicular glycogen, and sperm parameters improved in the Daflon-treated groups. Hence, pre-treatment with flavonoid fractions of diosmin and hesperidin mitigated CPF-induced reproductive toxicity.

Effects of Pinealectomy and Melatonin Supplementation on Elements Metabolism in Rat Testicular Tissue

Objective: The aim of this study was to investigate how pinealectomy and melatonin application affect elements metabolism in rat testicular tissue. Methods: The study was carried out on 32 adult male Spraque-Dawley rats. Animals were divided into 4 equal groups. Group 1: Control, Group 2: Melatonin, Group 3: Pinealectomy, Group 4: Pinealectomy+Melatonin. Group 2 and 4 animals received daily 3mg/kg intraperitoneal (ip) melatonin supplementation for 4 weeks. The pineal glands of Group 3 and 4 animals were removed under general anesthesia. At the end of the applications, testicular tissue samples were taken from the animals sacrificed under general anesthesia. Elemental determinations (µg/gram/tissue) were performed in testicular tissue samples using the atomic emission method. Results: The highest cobalt, molybdenum, nickel, manganese, phosphorus, and sodium levels (p<0.001) and the lowest potassium levels in the testicular tissue were obtained in the pinealectomy group (group 3) (p<0.001). Magnesium and selenium values in testicular tissue were highest in the pinealectomy group (group 3) (p<0.001), and were higher in the pinealectomy+melatonin group (group 4) than ingroup 1 (control) and group 2 (melatonin) (p<0.001). Testicular zinc levels were highest in group 2, where melatonin was administered, and lowest in group 3, which was the pinealectomy group (p<0.001). Conclusion: The findings obtained as a result of the study show that pinealectomy significantly disrupts element metabolism in the testicular tissue of rats, and melatonin supplementation may have a regulatory effect on testicular elemental metabolism.

Effects of oral exposure to iron oxide nanoparticles on reproductive system of male rats

To investigate the effects of oral exposure to iron oxide nanoparticles(Fe_2O_3NPs) on the reproductive system of male rats. Forty male SD rats were randomly divided into control group and low, medium, high dose groups, 10 rats in each group, normal saline and 50, 100 and 200 mg/kg Fe_2O_3NPs suspension were given by gavage, respectively. The volume of gavage was 10 mL/kg for 28 days. The body weight was weighed every three days, and the body weight changes of rats were recorded. After intraperitoneal anesthesia with 10% chloral hydrate, the rats were sacrificed by cervical dislocation, and the testis and epididymis were collected. Weigh and calculate the testicular coefficient and epididymal coefficient, the pathological sections of rat testis were observed by hematoxylin-eosin staining, the number of epididymal sperm was counted under an optical microscope and the sperm deformity rate was calculated. The activities of acid phosphatase(ACP), alkaline phosphatase(AKP), lactate dehydrogenase(LDH) and γ-glutamyl transpeptidase(γ-GT), the activity of superoxide dismutase(SOD), and the contents of glutathione(GSH) and malondialdehyde(MDA) in rat testis homogenate were detected by kit method. Compared with control group, there was no significant difference in body weight, testicular coefficient and epididymal coefficient in each dose group. In the medium and high dose groups, the arrangement of spermatogenic epithelium was disordered and spermatogenic cells decreased. The number of sperm in high dose group was decreased, and the sperm deformity rate in medium and high dose groups was increased(P<0.01). The activity of ACP in medium and high dose groups increased(P<0.05), and the activity of γ-GT decreased(P<0.01). There was no significant change in the activity of AKP and LDH in testicular homogenate of rats in each group(P>0.05). The level of GSH in medium dose group was increased(P<0.05), and the content of MDA in medium and high dose groups was increased(P<0.01). There was no significant difference in SOD activity among the groups(P>0.05). Under the conditions of this experiment, Fe_2O_3NPs can cause damage to the structure of rat testicular tissue, reduce the number of sperm, increase the rate of sperm deformity, interfere with the activity of marker enzymes in testicular tissue and induce oxidative stress injury, which has a negative impact on the reproductive system of male rats.

Protective effects of naringin on colistin-induced damage in rat testicular tissue: Modulating the levels of Nrf-2/HO-1, AKT-2/FOXO1A, Bax/Bcl2/Caspase-3, and Beclin-1/LC3A/LC3B signaling pathways.

Antimicrobial agent resistance has become a growing health issue across the world. Colistin (COL) is one of the drugs used in the treatment of multidrug-resistant bacteria resulting in toxic effects. Naringin (NRG), a natural flavonoid, has come to the fore as its antioxidant, anti-inflammatory, and antiapoptotic activities. The aim of the present study was to determine whether NRG has protective effects on COL-induced toxicity in testicular tissue. Thirty-five male Spraque rats were randomly divided into five groups (n = 7 per group): Control, COL, NRG, COL + NRG 50, COL + NRG 100. COL (15 mg/kg b.w., i.p., once per/day), and NRG (50or 100 mg/kg, oral, b.w./once per/day) were administered for 7 days. The parameters of oxidative stress, inflammation, apoptosis, and autophagic damage were evaluated by using biochemical, molecular, western blot, and histological methods in testicular issues. NRG treatment reversed the increased malondialdehyde level and reduced antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione) levels due to COL administration (p < 0.001), and oxidative stress damage was mitigated. Nuclear factor erythroid 2-related factor-2 pathway, one of the antioxidant defence systems, was stimulated by NRG (p < 0.001). NRG treatment reduced the levels of markers for the pathways of apoptotic (p < 0.001) and autophagic (p < 0.001) damages induced by COL. Sperm viability and the live/dead ratio were reduced by COL but enhanced by NRG treatment. Testicular tissue integrity was damaged by COL but showed a tendency to improve by NRG. In conclusion, COL exhibited toxic effect on testicular tissue by elevating the levels of oxidative stress, apoptosis, autophagy, inflammation, and tissue damage. NRG demonstrated a protective effect by alleviating toxic damage.

Umbilical Cord–Derived Mesenchymal Stem Cells Improve Ornidazole‐Induced Asthenozoospermia in Rats via Activation of the AKT/mTOR Pathway

Objective: Mesenchymal stem cells (MSCs) have been highly confirmed for their critical role in the treatment of different diseases. This study focuses on the mechanism of umbilical cord–derived MSCs (UC‐MSCs) in the treatment of ornidazole (ORN)‐induced asthenozoospermia (AS) in rats via the AKT/mTOR pathway.Methods: An animal model of AS was established in ORN‐induced rats, followed by treatment of UC‐MSCs and rapamycin (autophagy activator) or MK‐2206 (AKT inhibitor). The sperm motility, concentration, and viability of rats were measured by an automatic sperm analyzer. Hematoxylin and eosin (HE) staining was conducted to observe the pathological injury of testicular tissue in rats. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was utilized to evaluate the apoptosis rate of testicular cells. Western blot analysis was performed to determine the expression of apoptosis‐related proteins, autophagy‐related proteins, and AKT, p‐AKT, mTOR, and p‐mTOR. The rate of light chain 3 (LC3)–positive cells in testicular tissue was detected by immunohistochemistry (IHC).Results: In ORN‐induced AS rats, sperm motility, concentration, and viability as well as the number of mesenchymal cells and spermatogenic cells were significantly decreased, spermatogenic tubule space, apoptosis rate, and cleaved caspase‐3, LC3II/I, Beclin‐1, and LC3‐positive cell rates were increased, and Bcl2 was downregulated. UC‐MSCs could improve sperm quality and testicular injury in AS rats by inhibiting excessive autophagy. Besides, UC‐MSCs could activate the AKT/mTOR pathway. Moreover, inhibition of the AKT/mTOR pathway partially reversed the therapeutic effect of UC‐MSCs on ORN‐induced AS rats.Conclusion: UC‐MSCs inhibit autophagy and improve sperm quality in AS rats through the AKT/mTOR pathway, highlighting a new idea for the treatment of AS.

Roles of Cyt-c/Caspase-9/Caspase-3/Bax/Bcl-2 pathway in Cd-induced testicular injury in rats and the protective effect of quercetin

Cadmium (Cd) exposure causes oxidative damage to mitochondria, which would adversely affect rat testicular tissue. Quercetin (Que) is a natural antioxidant with anti-inflammatory, antioxidant and anti-apoptotic effects. However, the mechanism by which Que inhibits Cd-induced apoptosis of testicular cells remains unclear. The purpose of this study was to investigate the role of mitochondrial apoptosis pathway (Cyt-c/Caspase-9/Caspase-3/Bax/Bcl-2 pathway) in inhibiting Cd-induced apoptosis of testicular cells by Que. We used SD rats to simulate Cd chloride exposure by treating all sides of the rats with CdCl2 and/or Que. The levels of GSH and MDA in rat testis were detected using reagent kits. The effects of CdCl2 and/or Que on tissue damage, apoptosis, and gene and protein expression of the Cyt-c/Caspase-9/Caspase-3/Bax/Bcl-2 pathway in rat testis were examined by HE, TUNEL, RNA extraction and reverse-transcriptase polymerase chain reaction (RT-PCR), and Western blot (Wb). The results show that Cd significantly increased the contents of GSH and MDA in rat testis (P < 0.01); conversely, Que significantly reduced the contents of GSH and MDA (P < 0.01). Cd inflicted damage to testicular tissue, and Que addition significantly reduced the damage. Cd increased the number of apoptosis of testicle cells, and Que inhibited testicle-cell apoptosis. In addition, the results of reverse transcription PCR and Wb assays confirmed that, as expected, Cd increased the expression levels of Cyt-c, Caspase-9, Caspase-3, and Bax mRNAs as well as proteins. And at the same time decreased the expression of the anti-apoptotic factor Bcl-2 in the cells. Surprisingly, these effects were reversed when Que was added. Therefore, Que can play an antioxidant and anti-apoptotic role in reducing the testicular tissue damage caused by Cd exposure. This provides a conceptual basis for the later development and utilization of Que as well as the prevention and treatment of tissue damage caused by Cd exposure.

Effects of Exposure to Radiofrequency at 2.45 GHz on Structural Changes Associated with Lipid Peroxidation in Prepubertal Rat Testicular Tissue

Objective: The increasing use of electronic devices, accompanied by advancing technologies, has led to heightened exposure to non-ionizing electromagnetic radiation (EMR). This exposure instigates the accumulation of free radicals and oxidative damage in tissues, consequently impacting biological systems. Notably, the testis is among the tissues adversely affected by EMR. Numerous studies have highlighted the pivotal role of the testis in sperm production, emphasizing the potential implications of any damage on the reproductive system. This study aims to assess the levels of lipid peroxidation through histological evaluation in the testicular tissue of prepubertal male rats exposed to electromagnetic radiation at varying electric field intensities within the 2.45 GHz radiofrequency (RF) range. Methods: The experimental group comprises six subdivisions, including a sham control group, as well as groups exposed to varying electric field strengths (EFS) of 0.6 V/m, 1.9 V/m, 5 V/m, 10 V/m, and 15 V/m, respectively. Excluding the sham control group, the remaining subgroups were subjected to a daily 2.45 GHz RF exposure for 1 hour starting immediately after fertilization. This exposure to different electric field intensities continued for 45 days post-birth. Results: The samples obtained from the RF radiation-exposed rats exhibited elevated malondialdehyde (MDA) values and decreased glutathione (GSH) values in the testicular tissue. Furthermore, a comparative analysis between the microwave radiation-exposed group and the control group revealed distinct histological alterations in the testicular tissue. Conclusion: In conclusion, our findings indicate that exposure to microwave radiation at an electric field intensity of 15 V/m can lead to significant histopathological and oxidative parameter changes in Wistar rats. These results underscore the potential effects of such exposure on human health.

Role of parthenolide in paclitaxel-induced oxidative stress injury and impaired reproductive function in rat testicular tissue

The chemotherapeutic agent paclitaxel (PTX) causes testicular toxicity due to oxidative stress. Parthenolide (PTL), the active ingredient of the Tanacetum parthenium plant, is used to treat inflammation, dizziness, and spasms. In the present study, we evaluated the therapeutic effect of PTL on PTX-induced testicular toxicity in rats and its role in reproductive function. To this end, 6 groups were formed: control, PTX, sham, T1, T2, and T3. After testicular toxicity was induced in rats with 8 mg/kg PTX, the rats were treated with 1 mg/kg, 2 mg/kg, and 4 mg/kg PTL for 14 days. GSH and MDA levels were measured in rat testicular tissue after the last dose of PTL was administered. To determine the damage caused by PTX to testicular tissue by detecting 8-OHdG and iNOS, sections were prepared and examined histopathologically and immunohistochemically. Furthermore, the gene expressions and enzymatic activities of SOD, CAT, GPx, GST, and GR were investigated in all groups. After PTL treatment, MDA, 8-OHdG, and iNOS levels decreased while GSH levels increased in testicular tissue. Increased levels of antioxidant genes and enzymes also reduced oxidative stress. Additionally, the expression levels of the Dazl, Ddx4, and Amh genes, which are involved in gametogenesis and sperm production, decreased in case of toxicity and increased with PTL treatment. The data from this study show that PTL may have a therapeutic effect in the treatment of testicular damage by eliminating the oxidative stress-induced damage caused by PTX in testicular tissue, providing an effective approach to alleviating testicular toxicity, and playing an important role in reproduction/sperm production, especially at a dose of 4 mg/kg.

Gentisic acid ameliorates cisplatin-induced reprotoxicity through suppressing endoplasmic reticulum stress and upregulating Nrf2 pathway

Reproductive toxicity is a serious side effect of cisplatin (CP) chemotherapy. Gentisic acid (GTA) is a phenolic acid with strong antioxidant properties. Here, we aimed to determine therapeutic effect of GTA against CP-induced testicular toxicity in rats for the first time. Male Sprague-Dawley rats received a single dose of CP (5 mg/kg; intraperitoneal) and treated with GTA (1.5 and 3 mg/kg; intraperitoneal; 3 consecutive days). The levels of oxidative stress (OS), inflammation, endoplasmic reticulum stress (ERS) and apoptosis biomarkers were assessed in the testicular tissue of rats. In addition, how CP affects the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway and the effect of GTA on this situation were also addressed in the testicular tissue. CP administration induced histopathological changes in testicular tissue of rats with a significant increase in OS, inflammation, ERS and apoptosis biomarkers and a decrease in antioxidant capacity and Nrf2 expression levels. Administrations of GTA resulted in an amelioration of these altered parameters. These data suggest that GTA may be a potential therapeutic agent against CP-induced testicular toxicity. Activation of the Nrf2 pathway plays a key role of this therapeutic effect of GTA.