Introduction
Gamma radiation is a form of ionizing radiation that produces a wide range of biological effects. Characterized by high-energy photons capable of ionizing atoms, gamma radiation can induce DNA breaks, damage cell membranes, and cause chromosomal abnormalities [1]. Because of these properties, gamma radiation is widely used in industry, medicine, space science, and scientific research. In medical fields, particularly oncology, radiotherapy and gamma knife surgery rely on gamma radiation to selectively target and destroy malignant cells, which can lead to substantial physiological and morphological changes in the body [2]. However, gamma radiation also exerts harmful effects on healthy tissues, especially the gonads. Studies have shown that exposure to gamma radiation can cause sperm damage, including mitochondrial defects, and can trigger apoptosis in germ cells. For example, Li et al. [1] reported in their study on Linnaeus that cobalt-60 (⁶⁰Co-γ) radiation induces mitochondrial damage at the tip of the sperm tail and promotes apoptosis in germ cells [3]. Similarly, Hamza et al. [2] found that while a 150 Gy dose of gamma radiation led to regression in spermatogenesis, reduced sperm bundles, and dispersion within testicular tubules, doses of 50 and 100 Gy did not produce significant toxicological effects [4]. In addition, another study demonstrated damage to testicular tissues that were not directly irradiated but were instead affected by scattered or reflected rays during treatment, underscoring the testicles’ extreme sensitivity to gamma radiation [5].
To mitigate the harmful effects of gamma radiation, particularly during cancer therapy, antioxidants are frequently employed. These compounds enhance the body’s resistance to oxidative stress by neutralizing reactive oxygen species [6]. Among the antioxidants under investigation, myricitrin (Myc) and chebulinic acid (Che) have attracted considerable interest. Myc is a naturally occurring flavonoid found in fruits, vegetables, and tea. It has demonstrated strong antioxidant activity even at low concentrations [7] and possesses notable anti-carcinogenic properties [8]. Moreover, Myc appears to alleviate oxidative stress by upregulating the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway, increasing endogenous antioxidant levels, and helping to reduce hyperglycemia-induced oxidative injury. It has also been shown to inhibit nuclear factor kappa B (NF-κB) pathways involved in cardiac inflammation [9]. These properties make Myc a promising candidate for reducing radiation-induced damage in patients undergoing radiotherapy.
Che is an ellagitannin derived from the fruit of Terminalia chebula, a plant long used in traditional medicine. Its extract contains bioactive compounds such as tannins, phenolic acids, and flavonoids, which confer anti-diabetic, anti-inflammatory, antioxidant, hepatoprotective, neuroprotective, and gastroprotective effects [10]. Among these compounds, Che exhibits hepatoprotective activity by alleviating liver damage caused by toxins, alcohol, or other harmful agents, thereby supporting liver health and function [11].
Both Myc [12] and Che have also been shown to exert anti-inflammatory effects, in part by modulating tumor necrosis factor-α (TNF-α)-mediated inflammatory responses [13]. In this context, bioinformatics provides a valuable framework for elucidating the molecular mechanisms underlying gamma radiation-induced testicular injury. Through bioinformatic analyses, it is possible to investigate gene expression changes, protein interactions, and alterations in signaling pathways, particularly those associated with TNF-α-driven inflammation, in testicular tissues exposed to radiation.
To evaluate testicular damage at a structural level, stereological methods are essential. These techniques provide accurate three-dimensional quantification of testicular architecture, including seminiferous tubules, Leydig cells, and spermatogenic cell populations [14]. In experimental studies, stereology offers a powerful tool for detecting subtle morphological changes that traditional two-dimensional methods may overlook, making it especially valuable in assessing testicular damage [15]. Prior studies have used stereology to evaluate testicular structure in contexts such as obesity [15] and exposure to environmental toxicants [16], yet there remains a lack of stereological investigations specifically examining gamma radiation-induced testicular injury [15,16].
Therefore, this study aimed to investigate the protective effects of Myc and Che against gamma radiation-induced testicular damage, using stereological techniques and bioinformatic approaches focused on TNF-α-associated inflammatory pathways.
Methods
1. Experimental animals and procedures
1) Experimental animals
A total of 36 healthy 12-week-old male Wistar Albino rats were used in the study. The animals were housed under standard laboratory conditions, including a 12-hour light/dark cycle, a temperature of 22±2 °C, and a relative humidity of 55%±5%, with ad libitum access to food and water.
2) Experimental design
The rats were randomly assigned to six groups, with six animals in each group: (1) Control (Cont): No treatment was applied; (2) Gamma: Exposed to 16 mGy of gamma radiation for 1 hour daily for 10 consecutive days; (3) Myc: Received an intraperitoneal (i.p.) injection of Myc at a dose of 0.033 mg/kg once daily for 10 days; (4) Che: Received an i.p. injection of Che at a dose of 0.033 mg/kg once daily for 10 days; (5) Gamma+Myc: Exposed to 16 mGy of gamma radiation for 1 hour daily for 10 days, followed by an i.p. injection of 0.033 mg/kg Myc each day; and (6) Gamma+Che: Exposed to 16 mGy of gamma radiation for 1 hour daily for 10 days, followed by an i.p. injection of 0.033 mg/kg Che each day.
3) Radiation exposure
Gamma radiation exposure was performed using a mixed-source irradiator containing cesium-137 (¹³⁷Cs) and cobalt-60 (⁶⁰Co) radioisotopes. During irradiation, the rats were placed in a Plexiglas chamber to ensure uniform exposure. The procedure was conducted at the Physics Department of Ondokuz Mayis University.
4) Tissue collection
On the 11th day, 24 hours after the final treatment, all animals were anesthetized with i.p. injections of ketamine (80 mg/kg) and procaine hydrochloride (10 mg/kg). Intracardiac perfusion was then carried out using 4% paraformaldehyde in phosphate-buffered saline (PBS) for tissue fixation. The entire experimental process is illustrated in Figure 1. Following perfusion, the testicular tissues were carefully dissected and collected for subsequent histological and stereological analyses.
2. Routine tissue procedures and histological analysis
The collected testicular tissues were immediately fixed in 4% paraformaldehyde. Following fixation, the tissues were dehydrated using a graded alcohol series, cleared in xylene, and embedded in fresh paraffin blocks. Serial sections with a thickness of 7 μm were obtained using a rotary microtome. The sections were mounted on glass slides and stained with hematoxylin and eosin for general histological evaluation. Microscopic examination was performed using an Olympus CX41 light microscope (Olympus). The morphological characteristics of the seminiferous tubules, germinal epithelium, and Leydig cells were examined in all groups.
1) Immunohistochemical analysis
Immunohistochemical staining was performed to assess the expression of TNF-α in testicular tissues. An anti-TNF-α primary antibody (Abcam, ab6671; Kimera Medical) was used. Five-micrometer-thick paraffin sections were prepared and deparaffinized before staining.
The sections were incubated in 3% hydrogen peroxide (H₂O₂) for 10 minutes to block endogenous peroxidase activity. They were then blocked with 5% bovine serum albumin for 10 minutes at room temperature. The primary antibody was applied, and the sections were incubated at 36 °C for 2 hours.
After incubation, the sections were washed three times with PBS, followed by incubation with a biotinylated anti-rabbit immunoglobulin G secondary antibody for 20 minutes at 37 °C. Visualization of the immune complex was achieved using the streptavidin–biotin–peroxidase complex method (ScyTek Research Facilities; Sito-Gen Biomedikal Ltd.), with diaminobenzidine tetrahydrochloride (DAB) serving as the chromogen. Mayer’s hematoxylin was used for counterstaining.
Stained slides were examined using a camera-equipped research microscope (Olympus CX41; Olympus). TNF-α immunoreactivity was evaluated in the seminiferous epithelium and interstitial regions of the testicular tissue.
3) Volumetric analyses
Volumetric estimations of the testes (total volume) and seminiferous tubules were performed using the Cavalieri method. This method estimates volume by analyzing parallel sections taken at equal distances. The surface area of each section in the same orientation is determined, and multiplying this area by the section thickness yields the sectional volume. Summing the sectional volumes provides the total volume of the structure. Mathematically, this is expressed as:
where Vt represents the total volume of the structure of interest, t is the section thickness, and A is the measured area.
For volumetric analysis, images were captured from testicular samples using a camera-attached microscope at ×4 magnification for total testis volume and ×10 magnification for seminiferous tubule volume. Approximately 20–25 sections and 100–150 images were obtained from each testis. The images were analyzed in the ImageJ program (National Institutes of Health), where a dotted area ruler with an area of 0.25 cm² was superimposed. Point counting on the grid was used for volumetric estimation.
3. Estimation of the numbers in the germinal epithelium and interstitial cells of testes (Leydig cells)
The physical disector method was used to estimate the mean numbers of spermatogonia, spermatocytes, and spermatids in the germinal epithelium, as well as Leydig cells in the interstitial space between seminiferous tubules. Serial section pairs (two sequential sections) were examined to identify corresponding counting areas. Photographs of disector pairs (two images of identical anatomical areas) were taken based on reference points such as blood vessels and coordinates within the sections. An unbiased counting frame was placed on the image pairs, and cells falling within the countable area were enumerated. Counting in the section pairs followed these criteria.
Inclusion criteria: (1) Only nuclei of cells that are completely within the unbiased counting frame or along the permitted inclusion borders were counted; (2) If a nucleus was visible in the reference section but absent in the look-up section, it was counted as a disector particle.
Exclusion criteria: (1) Any nucleus that appeared in both sections was not counted; (2) A nucleus visible only in the reference section was not counted if it was located on the forbidden lines or outside the counting frame.
The distance between the serial sections was considered the disector height, and the number of disector particles was determined across this height [15,16]. The values were estimated according to acceptable coefficient of error limits [17]. Tissue shrinkage and microscope magnification (×400) were also included in the disector volume calculations.
To determine tissue shrinkage, the volumes of fresh testes (Vft) were measured using the water immersion method. After tissue processing, the final testis volumes (Vlt) were estimated using the Cavalieri principle on stained tissue sections.
Shrinkage from fresh tissue to the final processed block was calculated using the following formula:
Based on all calculations, the area of the unbiased disector frame in this study was 8×8 cm on the screen (corresponding to 0.25 mm² in actual size). The disector height was determined as 7 μm, and the counting frame volume was calculated as 0.025 mm³. A pilot study was performed following this plan. Once an acceptable error coefficient was achieved using 25 disector pairs and the predetermined disector height and volume values, it was decided to proceed with this methodology for the full study.
After completion of all counting procedures, the mean number of cells per cubic millimeter was calculated using the following formula:
4. Bioinformatical analysis
In the bioinformatics analysis, the effects of radiation on TNF-α and related pathways were examined. Protein–protein interaction data were obtained from the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database. To determine activation levels of radiation-associated pathways linked to TNF-α (e.g., transforming growth factor-β signaling, NF-κB activation, apoptosis, and inflammatory pathways), Gene Set Enrichment Analysis (GSEA) was performed. This analysis detailed the changes in the activation of TNF-α–associated pathways in response to radiation exposure. Interaction networks were visualized using Cytoscape software, and radiation-induced alterations within these networks were assessed. Interaction scores were determined using a high-confidence threshold (0.900).
5. Statistical analysis
Statistical analyses were performed using SPSS ver. 21.0 software for Mac (IBM Corp.). The results are presented as mean±standard deviation. Normality tests were conducted prior to analysis to determine whether the data were normally distributed. One-way analysis of variance, the Tukey test, and the Kruskal-Wallis test were used to compare differences among the groups.
6. Ethics approval
All experimental procedures were conducted in accordance with ethical guidelines for animal research, and approval was obtained for the histopathological and stereological evaluation of cadaveric tissues (not included in the scope of the project) from animals used in the project numbered 2014/41, approved by the Local Ethics Committee for Animal Experiments of Ondokuz Mayis University.
Results
1. Stereological results
1) Volume of the testes
The testis volume in the gamma group was significantly lower than that of the Cont group (p<0.01). In contrast, the testis volumes of the Che and Myc groups did not differ from the Cont group (p>0.05). In both groups treated with antioxidants in addition to gamma radiation, testis volume increased relative to the gamma group (p<0.05) (Figure 3A).
2) Volume of the seminiferous tubules
The seminiferous tubule volume in the gamma group showed a significant decrease compared with the Cont group (p<0.01). However, the seminiferous tubule volumes of the Che and Myc groups were not significantly different from those in the Cont group (p>0.05). In both antioxidant-treated groups following gamma exposure, an increase was observed compared with the gamma group. A statistically significant increase, however, was detected only in the gamma+Myc group (p<0.05) (Figure 3B).
3) Mean number of spermatogonia
The number of spermatogonia in the gamma group decreased significantly compared with the Cont group (p<0.01). Although the Che and Myc groups showed higher values than the Cont group, these increases were not statistically significant (p>0.05). In both groups treated with antioxidants after gamma exposure, an increase was observed compared with the gamma group, but a statistically significant difference was detected only in the gamma+Myc group (p<0.01) (Figure 3C).
4) Mean number of spermatocytes
The results showed that the number of spermatocytes in the gamma group decreased significantly compared with the Cont group (p<0.05). In the Myc group, the number of spermatocytes increased slightly relative to the Cont group, although this difference was not significant (p>0.05). In the groups treated with antioxidants following gamma exposure, increases were observed compared with the gamma group, with statistical significance again observed only in the gamma+Myc group (p<0.05) (Figure 3D).
5) Mean number of spermatids
A decrease in the number of spermatids was observed in the gamma group compared with the Cont group (p<0.05). When comparing the Cont, Che, and Myc groups, the Myc group showed a significant increase in spermatid number compared with both the Cont (p<0.05) and Che (p<0.05) groups. In comparing the gamma and gamma+Myc groups, the gamma+Myc group demonstrated a significant increase in spermatids (p<0.01) (Figure 3E).
6) Mean number of Leydig cells
Analysis of Leydig cell numbers showed a significant decrease in the gamma group compared with the Cont group (p<0.01). In both the gamma-Myc and gamma-Che groups, the number of Leydig cells increased relative to the gamma group (p<0.05) (Figure 3F).
2. Histopathological results
In the examination of the testes in the control group, the seminiferous tubules, interstitial connective tissue, and Leydig cells displayed a normal histological appearance. Cells of the spermatogenic series were regularly arranged along the tubule wall. The interstitial connective tissue occupying the spaces between the tubules and the Leydig cells exhibited normal morphology (Figure 4 Cont/I–IV). Spermatogonia in the germinal epithelium had heterochromatic round nuclei located on the basal lamina. Primary spermatocytes were identifiable by their prominent oval nuclei and abundant cytoplasm. Spermatids had small, darkly stained nuclei situated near the lumen. Late spermatids and immature spermatozoa were present in the lumen with long, spindle-shaped nuclei. Leydig cells, typically polygonal, exhibited a smooth, oval-shaped nucleus (Figure 4 Cont/II–IV).
In the evaluation of the Che and Myc groups, the testes showed a morphology similar to that of the control group. The germinal epithelium appeared regular, and epithelial cells were healthy. The interstitial area maintained normal structure, and Leydig cells also displayed normal histological features (Figure 4 Myc/I–IV).
In the gamma group, marked damage was observed in the seminiferous tubules and spermatogenic cells. Atrophy of the seminiferous tubules and reductions in spermatogenic cell layer thickness and cellular continuity were evident compared with the control group. The interstitial connective tissue was also diminished (Figure 4 gamma/I–II). Vacuolar degeneration was detected in nearly all layers of the germinal epithelium (Figure 4 gamma/II inset) as well as in Leydig cells (Figure 4 gamma/IV). Both spermatogonia and primary spermatocytes were reduced in number relative to the control group, and many cells exhibited irregular, circumscribed, pyknotic nuclei. Spermatids, located near the lumen, had small, darkly stained nuclei and were markedly fewer in number (Figure 4 gamma/III–IV).
In the histopathological examinations of the gamma-Myc group, the seminiferous tubule morphology and germinal epithelium were noticeably improved compared with the gamma group. The cells displayed typical histological features, and the interstitial connective tissue was rich in cellular components (Figure 4 gamma-Myc/I–IV). Increased mitotic activity was observed, and dividing cells were readily identified (Figure 4 gamma-Myc/III).
In the histopathological evaluation of the gamma-Che group, the seminiferous tubules, interstitial connective tissue, and Leydig cells exhibited a healthier appearance than in the gamma group. The tubule wall had a more regular organization, and the spermatogonia were more densely arranged and smaller than those in the gamma group. The interstitial connective tissue appeared normal, and Leydig cells contained cytoplasmic regions rich in presumed lipid droplets (Figure 4 gamma-Che/I–IV).
3. Immunohistochemical results
In the Cont, Myc, and Che groups, no TNF-α positivity was detected along the seminiferous tubule wall. In contrast, the testis sections from rats in the gamma group showed strong TNF-α positivity in the cytoplasm of spermatogonia, spermatocytes, and spermatids. However, following Myc and Che administration to rats exposed to gamma radiation, TNF-α positivity in the seminiferous tubule walls decreased markedly. This reduction was evident across the germinal epithelium and appeared substantially lower than in the gamma group alone (Figure 5).
4. Bioinformatic results
The bioinformatic analyses determined that the factors integrin beta-1 receptor (ITGB1), X-ray radiation resistance-associated protein 1 (XRRA1), RB1-inducible coiled-coil protein 1 (RB1CC1), radiation-inducible immediate-early gene IEX-1 (IER3), and TNF were involved in various cellular processes, such as cell signaling, autophagy, DNA repair, and immune responses. These proteins can interact through multiple mechanisms, particularly within contexts such as radiation response, inflammation, and stress-associated pathways. X-ray radiation resistance-associated protein 1 (XRRA1) is known to participate in cellular responses to radiation-induced damage, likely influencing resistance to DNA breaks caused by ionizing radiation. After radiation exposure, XRRA1-mediated resistance may involve ITGB1 in regulating cell adhesion and migration during tissue repair. XRRA1 may also affect cytokine expression, including TNF, thereby modulating inflammatory responses triggered by radiation. RB1CC1 plays a central role in autophagy, supporting cell survival under conditions of DNA damage and radiation-induced stress. This factor may interact with both IER3 and TNF within integrated survival and repair pathways. IER3 can act as an important mediator of cell survival by modulating extracellular signal-regulated kinase (ERK) signaling and inhibiting apoptosis, interacting functionally with RB1CC1 and TNF in response to cellular stress. TNF itself functions as a key regulator of inflammation and cell death, influencing adhesion via ITGB1 and participating in survival pathways such as autophagy mediated by RB1CC1 and IER3. TNF may initiate cellular programs that involve ITGB1-associated adhesion mechanisms and RB1CC1-driven autophagic activity. The TNF-mediated inflammatory response may promote tissue repair processes while concurrently activating survival pathways through IER3 and RB1CC1 to limit apoptosis. Overall, these factors appear highly interconnected, particularly in pathways associated with cellular stress responses, inflammatory signaling, and DNA damage repair. Their interactions are formed through gene neighborhood relationships, gene fusions, co-occurrence, co-expression patterns, and protein homology. Together, these connections suggest a coordinated molecular network influencing cellular survival, repair, and adaptation to environmental stressors such as radiation and inflammation (Figure 6).
Discussion
Gamma rays, a form of ionizing radiation, are widely used as therapeutic agents in various medical applications, particularly in cancer treatment. Gamma radiation increases oxidative stress parameters within cells and induces DNA damage [18]. Although the extent of gamma radiation-induced injury varies depending on dose, it remains debated whether harmful effects occur even at doses below 10 cGy. Because gamma rays are highly ionizing, they are thought to contribute to the development of cancers and several other disorders [19]. Moreover, numerous studies on the male reproductive system have demonstrated that gamma radiation exerts destructive effects on testicular tissue [20-23]. For example, a 2017 study examining different gamma radiation doses in Culex pipiens reported rupture, necrosis, and degeneration in the testicular wall, as well as abnormal distribution of spermatogonial and spermatocytic developmental stages, ultimately leading to a reduction in spermatogenesis [24]. Similarly, a 2,022 study investigating gamma radiation effects in mice showed increased cell death within the male reproductive system and decreased spermatogenesis [25].
In the present study, male rats were exposed to 16 mGy of radiation for 10 days, and their testicular tissues were subsequently examined. Stereological analyses revealed reductions in seminiferous tubule volume and in the mean numbers of spermatogonia, spermatocytes, spermatids, and Leydig cells in the gamma group compared with the control group. Examination of testicular samples from the gamma group showed seminiferous tubules with smaller volume, scattered morphology, and marked gaps along the tubule walls.
Many studies suggest that the harmful effects of gamma radiation occur primarily through oxidative stress mechanisms [26]. Therefore, this study aimed to evaluate the potential protective effects of Myc and Che—two bioactive compounds with high antioxidant capacities—on testicular damage caused by gamma radiation.
Recent studies have demonstrated that Myc attenuates inflammation and apoptosis in diabetic cardiomyopathy by suppressing Nrf2 activation and NF-κB signaling. Likewise, in models of hyperglycemia-induced oxidative stress, Myc increases the activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) and reduces lipid peroxidation [9]. Che has been shown to exhibit antioxidant [27], antibacterial [28], and anti-apoptotic [29] properties. Additional reports indicate that Che inhibits the proliferation of cancer cells, suggesting its potential utility in cancer prevention and treatment [6,30].
Although several studies have noted that Che used directly as a plant extract may negatively affect sperm morphology, induce hypo-testicular activity, and cause spermatogonial loss [8,31,32], no significant decrease in spermatogenic cells was observed in our study. This difference may be attributable to the dose used, as many published studies have employed considerably higher concentrations of Che. Indeed, one previous study reported no increase in sperm mortality at doses up to 0.1 mg/mL [32]. In the stereological analyses from the present study, numerical increases in spermatogonia, spermatids, and Leydig cells were observed in rats receiving Che following gamma radiation exposure. However, seminiferous tubule volume did not change significantly in the Che-treated rats exposed to gamma radiation.
When the effects of another antioxidant, Myc, on testicular damage were examined, it was observed that the seminiferous tubule volume of rats exposed to gamma radiation and subsequently treated with Myc was significantly higher than that of the gamma group and approached the level of the control group. Similarly, significant increases were detected in the numbers of spermatogonia, spermatocytes, spermatids, and Leydig cells. All of these estimations indicate that Myc exerts more beneficial effects than Che in both the control and gamma-exposed groups. A study conducted by Öztürk et al. demonstrated that Myc administered half an hour before detorsion had a dose-dependent protective effect in rats through antioxidant mechanisms [33]. They reported that the antioxidant properties of Myc reduce the harmful impact of reactive oxygen radicals on germ cells. Likewise, a 2021 study by Oroojan et al. [34] on diabetic mice showed that high-dose Myc increased the testicular volume that had decreased due to diabetes. The histopathological analyses in the present study further support these findings, demonstrating that seminiferous tubule and germinal epithelial morphologies damaged by gamma radiation improved following Myc treatment.
The bioinformatic analyses performed in the study showed that the oxidative stress elevated by gamma radiation was reduced when Myc was administered. In light of this information, it can be concluded that Myc reduces testicular damage primarily through its antioxidant system. These findings also illustrate how proteins such as ITGB1, XRRA1, RB1CC1, IER3, and TNF interact in various cellular processes, particularly in response to environmental stressors such as radiation and inflammation. In addition to these factors, the relationship between flavonoid compounds like Myc and Che and TNF-α plays a notable role in modulating inflammation and cellular stress responses. Both Myc and Che interact with TNF-α to regulate inflammatory pathways and influence cellular survival. By inhibiting the production and activity of TNF-α, these compounds may mediate interactions between TNF-α and proteins such as ITGB1 and RB1CC1, thereby affecting adhesion, autophagy, and other survival mechanisms. This suggests that Myc and Che could function as modulators of the molecular network governing cellular adaptation to radiation and inflammation. Their effects on TNF-α may enhance cell survival and repair mechanisms, offering protection against apoptosis induced by damage. Several studies have shown that Myc inhibits TNF-α production and modulates inflammatory responses. Specifically, Myc has been reported to suppress TNF-α-induced inflammatory signaling, suggesting that it may regulate TNF-α–mediated cell communication and influence the activity of proteins such as ITGB1, RB1CC1, and IER3 that participate in survival and repair processes [35]. This anti-inflammatory effect of Myc may have therapeutic implications for conditions such as cancer and cardiovascular disease, where TNF-α plays a significant role in disease progression. Research also indicates that Che can inhibit TNF-α production and reduce inflammatory responses [36]. The anti-inflammatory activity of Che is believed to be mediated through suppression of TNF-α and its downstream signaling pathways. This suggests that Che may influence cellular stress responses by affecting proteins such as ITGB1 and RB1CC1, ultimately supporting cellular survival and repair following injury.
All data indicate that Che and Myc reduce the destructive effects of gamma radiation on testicular tissue. Both antioxidants were found to enhance spermatogenesis when administered individually, and these effects likely contribute to their protective roles following gamma exposure. When the two antioxidants are compared, Myc appears to exert a more pronounced protective effect. Nevertheless, future studies are needed to evaluate the potential synergistic or additive effects of combined administration of Myc and Che in mitigating radiation-induced testicular injury.
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