Cadmium-induced Testicular Damage Research Articles

Therapeutic potential of the linalool against cadmium-induced testicular tissue damage

Cadmium (Cd) is a heavy metal that has harmful effects and is one of the contaminants found in the environment. Cd exposure causes important pathophysiological processes, such as reproductive toxicity. Linalool (Lnl) is a monoterpene, a component of essential oils known to be produced synthetically. Additionally, Lnl has many important beneficial effects, such as anti-inflammatory and antioxidant effects. The objective of this study is to determine whether Lnl has a healing impact in opposition to testicular tissue damage due to Cd exposure. In the study, 28 male rats were divided at random into four equal groups (n = 7). No treatment was applied to the control group. CdCl2 was applied intraperitoneally to the Cd group at a dose of 3 mg/kg for the first 7 days of the trial. For the Cd + Lnl group, 3 mg/kg CdCl2 was applied intraperitoneally for the first 7 days of the trial, and 100 mg/kg/day Lnl was applied. Upon completion of all applications, the rats were sacrificed and blood samples and testicular tissue were taken. Cd exposure caused histopathological changes, oxidative stress, inflammation, and an increase in apoptotic cells in testicular tissue. However, Cd altered endocrine hormones in the hypothalamic-pituitary-gonad axis. However, Lnl application against Cd exposure was able to regulate the negativity caused by Cd in both testicular tissue and endocrine hormone levels. In conclusion, Lnl may be a potential therapeutic strategy against Cd-induced reproductive toxicity. We believe that Lnl has a high potential for further studies to determine its detailed mechanisms of action and cellular signaling pathways.

The FAK/occludin/ZO-1 complex is critical for cadmium-induced testicular damage by disruption of the integrity of the blood-testis barrier in chickens

Cadmium (Cd) is a well-known testis toxicant. The blood-testis barrier (BTB) is a crucial component of the testis. Cd can disrupt the integrity of the BTB and reproductive function. However, the mechanism of Cd-induced disruption of BTB and testicular damage has not been fully elucidated. Here, our study investigates the effects of Cd on BTB integrity and testicular dysfunction. 80 (aged 1 day) Hy-Line white variety chickens were randomly designed into 4 groups and treated for 90 days, as follows: control group (essential diet), 35 Cd, 70 Cd and 140 Cd groups (35, 70 and 140 mg/kg Cd). The results found that Cd exposure diminished volume of the testes and induced histopathological lesions in the testes. Exposure to Cd induced an inflammatory response, disrupted the structure and function of the FAK/occludin/ZO-1 protein complex and disrupted the tight junction and adherens junction in the BTB. In addition, Cd exposure reduced the expression of steroid-related proteins and inhibited testosterone synthesis. Taken together, these data elucidate that Cd disrupts the integrity of the BTB and further inhibits spermatogenesis by dissociating the FAK/occludin/ZO-1 complex, which provides a basis for further investigation into the mechanisms of Cd-induced impairment of male reproductive function and pharmacological protection.

Cadmium-Induced Testicular Damage in Rats: Modulatory Role of Stemenhance® Against Oxidative Stress

Cadmium-Induced Testicular Damage in Rats: Modulatory Role of Stemenhance® Against Oxidative Stress

Silent Information Regulator 1 Mediates Quercetin Protective Effect on Cadmium-induced Testicular Damage in Adult Male Rats

Silent Information Regulator 1 Mediates Quercetin Protective Effect on Cadmium-induced Testicular Damage in Adult Male Rats

Evaluation of the Potential Protectivity of Both Allium sativum and Zingiber officinale on the Cadmium-Induced Testicular Damage in Rats.

Cadmium (Cd) is a widely spread environmental pollutant, listed among the unsafe metals due to known toxic effects on multiple organs, including the testes. In this study, we aim to evaluate the potential protectivity of garlic and ginger extracts on Cd-induced damage of the testis in rats. Fifty-six adult male albino rats were alienated into seven groups; control group, garlic-treated group, and ginger-treated group were given garlic and ginger extracts at doses of 250 mg and 120 mg/kg b.wt/day, Cd-treated group received 8.8 mg/Kg b.wt/day of Cd chloride, and the protected groups were given Cd and co-treated with garlic, ginger, or both extracts. The testes were subjected to different procedures to assess the oxidative status and histopathological changes. Cd-treated rats showed a significant reduction in the testis weight and morphometric measurements of the seminiferous tubules compared to the control group. Cd administration resulted in a marked drop in the testosterone level and activities of antioxidative enzymes. Moreover, Cd induced histopathological changes in the seminiferous tubules. Co-administration of garlic and ginger extracts with the Cd showed partial improvement in the investigated parameters toward the control figures and improvement in the morphological changes. Co-treating both extracts together and the Cd resulted in complete normalization of these adverse effects of Cd. These findings indicated that garlic and ginger extracts could ameliorate the harmful effects of Cd on the testis. This effect was more prominent when garlic and ginger extracts were co-administered together with Cd.

Combined apocynin and carvedilol protect against cadmium-induced testicular damage via modulation of inflammatory response and redox-sensitive pathways

Testicular damage is considered a severe complication of cadmium (Cd) exposure which is associated with tissue oxidative stress damage, inflammation, and apoptosis. The present study investigated the antioxidant, anti-inflammatory, and anti-apoptotic activities of apocynin (APO) and carvedilol (CVD) against Cd-induced acute testicular damage. Rats were allocated into five groups as follows: normal control (received vehicle), Cd control group (2 mg/kg, i.p), APO-treated group (25 mg/kg, P.O.), CVD-treated group (10 mg/kg, P.O.), and combination group (APO + CVD). Blood, serum, and tissue samples were withdrawn for hematological, biochemical, molecular, and histological analyses. The present results confirmed testicular damage after cd exposure as indicated by alteration of serum hormonal levels, hematological defects, histopathological changes, and loss of steroidogenic functions. Besides, Cd injection-induced up-regulation of NADPH oxidase, MDA, NF-κB, IRF3, MPO, pro-inflammatory cytokines, Bax, and cleaved caspase-3 expression concomitant with down-regulation of Nrf2, GSH, SOD, and Bcl2 expression. Interestingly, pretreatment with APO and/or CVD significantly relieved Cd-induced testicular damage at cellular and molecular levels. Notably, the combined protective effect of APO plus CVD was higher than the protective effect of each drug alone. Overall, combined APO and CVD could serve as a good candidate for protection against Cd-induced testicular damage via suppression of inflammatory response and modulation of the redox-sensitive pathway.

Mechanisms of Cadmium-Induced Testicular Damage

Mechanisms of Cadmium-Induced Testicular Damage

Caffeic acid phenethyl ester mitigates infertility: A crucial role of metalloproteinase and angiogenic factor in cadmium-induced testicular damage.

Cadmium (Cd) is expected to cause deleterious effects on most organs, especially on the male reproductive system. The current study was performed to assess the effect of Cd on fertility in Swiss mice and to evaluate the protective role of caffeic acid phenethyl ester (CAPE) in relieving the detrimental effect of Cd. The mice were divided into four groups of 10: normal Group I received distilled water. Group II, III, and IV were injected 3 mg/kg body weight with Cd intraperitoneally for four consecutive days. Group III received saline. Group IV was treated with 3 mg/kg/day CAPE intraperitoneally for 6 days. Results indicated that CAPE brings about a highly significant improvement in fertility parameters, spermatogenesis, and reduced apoptotic percent. Moreover, metalloprotease-3 (MMP-3) and vascular endothelial growth factor reduced significantly. Overall, our results strongly suggest that CAPE has a protective effect, counteracts the toxic effects of Cd, and prevents testicular injury.

Modulatory Role of Vitamin E on Proton Pump (ATPase) Activity of Cadmium Chloride-Induced Testicular Damage in Wistar Rats.

Proton pumps are membrane-bound enzymes important in generating gradients that help in maintaining cellular ion homeostasis, cell membrane potential, water, and solute transport across the cell surface. This study investigated the modulatory role of vitamin E on proton pump activity and reproductive parameters in cadmium-induced testicular damage. Twenty (20) male Wistar rats weighing between 180 and 200 g were sorted into 4 groups of five rats each. Group I served as the control and was given normal saline orally, Group II rats were treated with a single dose of 2 mg/kg BW cadmium chloride (CdCl2) intraperitoneally, Group III rats were given 100 mg/kg BW of vitamin E orally, and Group IV rats were given 100 mg/kg BW of vitamin E orally for 30 days prior to intraperitoneal administration of single dose of 2 mg/kg BW of cadmium chloride. The rats were anaesthetized with diethyl ether, and blood samples were obtained for sex hormonal analysis; caudal epididymis was dissected for sperm count, motility, and viability, and the testis were homogenized for lipid peroxidation and proton pump (Na+/K+ ATPase, Ca2+ ATPase, and Mg2+ ATPase) activity. Proton pump activity was assayed spectrophotometrically using the Stewart method to determine the inorganic phosphate level. Histopathological changes of the testis were also studied. The group treated with CdCl2 showed a significant (p < 0.05) decrease in proton pump activity, sperm count, and motility and a significant (p < 0.05) increase in malondialdehyde level when compared with the control group. The CdCl2-treated group also showed decrease reproductive organ weights and hormonal levels and cause necrosis of spermatogonia lining the seminiferous tubules. Rats treated with vitamin E orally for 30 days prior to CdCl2 exposure showed improvement in proton pump activity, a significant (p < 0.05) increase in sperm parameters and luteinizing hormonal level, and a decrease in the lipid peroxidation level as compared with the CdCl2 group. This study showed that vitamin E ameliorated the toxic effect of CdCl2 on proton pump activity in the testes, hence improving testicular integrity, structures, and functions.

Caffeine versus antioxidant combination (Antox) and their role in modifying cadmium-induced testicular injury in adult male albino rats.

The aim of the current work was to compare the roles of caffeine and antioxidants in prevention of cadmium-induced testicular damage when given, in addition to cadmium, in adult male albino rats. Histopathological and ultra-structural examination as well as biochemical and molecular assessments were done. Cadmium chloride (4mg/kg body weight) was administered via oral gavage from day 21 to 28 of the experiment. Caffeine (25mg/kg) via intra-peritoneal injection and antioxidant preparation (Antox) 10mg/kg via oral gavage were given as a pre-treatment for 21days and concomitantly with Cd from day 21 to 28. Real-time PCR was done for determination of 3, 17 β hydroxy steroid dehydrogenase steroidogenic acute regulatory protein, caspase-9 and mitofusin 1,2 gene expression. Testosterone level, glutathione S-transferase enzyme activity, reactive oxygen species, malondialdehyde and superoxide dismutase were measured spectrophotometrically by ELISA. Histological and ultra-structural evaluation revealed disturbance of normal architecture, vacuolisation and necrosis. Vascular dilatation and congestion and collagen fibre deposition were present. A statistically significant difference was seen in all parameters when caffeine and antioxidants were given against cadmium-induced testicular injury. Overall, we conclude that both caffeine and antioxidants have the ability to reverse cadmium-induced testicular injury when given as pre-treatment prior to cadmium exposure.

Protective Effect of Graviola (Annona muricata) Leaves Extract Against Cadmium-Induced Testicular Toxicity In Male Albino Rats

Graviola (Annona muricata), an edible plant belonging to the Annonaceae family, has a long history in traditional medicine due to its wide range of therapeutic effects on many ailments. This study was planned to assess the protective potentials of Graviola leaves extract (GLE) on cadmium-induced testicular damage in male albino rats. The study was conducted on 32 male adult Wistar rats randomly divided into four groups (n=8/each). A (control group); B (GLE, 100 mg/kg); C (cadmium chloride (CdCl2), 5 mg/kg) and D (GLE, 100 mg/kg + CdCl2 5 mg/kg). All administrations were performed by daily gavage for 8 weeks. Blood, testes, and epididymis were harvested for biochemical and histological investigations. In addition to sperm analysis, sperm DNA comet assay, and apoptotic indices. Results revealed that GLE significantly reversed (p < 0.05) testicular oxidative stress induced by CdCl2, maintained male sex hormones levels, and restored testis architecture via increasing the testicular antioxidant status. GLE co-treatment significantly increased (p < 0.05) sperm count, motility, viability, and DNA integrity along with significantly reducing sperm DNA damage and sperm head abnormality in comparison with CdCl2 group. Additionally, GLE protected germ cells from Cd-induced apoptosis. In conclusion, results of the present study confirmed that GLE has potent antioxidant potentials and cytoprotective capacity against the deleterious effects of CdCl2 on testicular tissue by reducing cellular oxidative stress prompted by the generation of the reactive oxygen species.

Protective effect of green tea extract against cadmium-induced testicular damage in rats in respect of oxidant/antioxidant equilibrium and androgen production

Objective: Investigating the effect of green tea extract (GTE) on the testicular damage induced by cadmium chloride CdCl2 in male rats. Design: Randomized controlled study. Animals: 40 male Wistar rats. Procedures: Rats were randomly divided into four groups: A) control group (each rat daily received pellet diet); B) GTE group each rat daily received pellet diet as well as 3 ml of 1.5 % w/v GTE, C) CdCl2 group each rat was I/P injected a single dose of 1 mg/kg CdCl2, then daily received pellet diet, and D) CdCl2+GTE group each rat was I/P injected a single dose of 1 mg/kg CdCl2 then daily received pellet diet as well as 3 ml of 1.5 % w/v GTE. After 30 days, blood samples were collected for hormonal assays (testosterone, FSH, and LH). In addition, both testes were collected; one of them was used for quantification of 17-beta hydroxysteroid dehydrogenase III (17β-HSDIII) gene expression using a real-time PCR. The other testis was used for determination of catalase and reduced glutathione; GSH, Nitric oxide (NO) and malondialdehyde (MDA) levels. Results: CdCl2 decreased serum testosterone levels and its synthesis pathway (17β-HSDIII testicular gene expression). While antioxidants catalase and GSH were reduced, oxidants MDA were enriched in the testes of CdCl2-poisoned rats. This CdCl2-promoted testicular dysfunction was corrected via the administration of GTE to male rats. Conclusion and clinical relevance: GTE could be used as a remedy for protecting against CdCl2-induced testicular damage in male rats.

Protective effect of green tea extract against cadmium-induced testicular damage in rats in respect of oxidant/antioxidant equilibrium and androgen production

Protective effect of green tea extract against cadmium-induced testicular damage in rats in respect of oxidant/antioxidant equilibrium and androgen production

Effects of Myo-inositol Alone and in Combination with Seleno-Lmethionine on Cadmium-Induced Testicular Damage in Mice.

Cadmium (Cd) impairs gametogenesis and damages the blood-testis barrier. As the primary mechanism of Cd-induced damage is oxidative stress, the effects of two natural antioxidants, myo-inositol (MI) and seleno-L-methionine (Se), were evaluated in mice testes. Eighty-four male C57 BL/6J mice were divided into twelve groups: 0.9% NaCl (vehicle; 1 ml/kg/day i.p.); Se (0.2 mg/kg/day per os); Se (0.4 mg/kg/day per os); MI (360 mg/kg/day per os); MI plus Se (0.2 mg/kg/day); MI plus Se (0.4 mg/kg/day); CdCl2 (2 mg/kg/day i.p.) plus vehicle; CdCl2 plus MI; CdCl2 plus Se (0.2 mg/kg/day); CdCl2 plus Se (0.4 mg/kg/day); CdCl2 plus MI plus Se (0.2 mg/kg/day); and CdCl2 plus MI plus Se (0.4 mg/kg/day). After 14 days, testes were processed for biochemical, structural and immunohistochemical analyses. CdCl2 increased iNOS and TNF-α expression and Malondialdehyde (MDA) levels, lowered glutathione (GSH) and testosterone, induced testicular lesions, and almost eliminated claudin-11 immunoreactivity. Se administration at 0.2 or 0.4 mg/kg significantly reduced iNOS and TNF-α expression, maintained GSH, MDA and testosterone levels, structural changes and low claudin-11 immunoreactivity. MI alone or associated with Se at 0.2 or 0.4 mg/kg significantly reduced iNOS and TNF-α expression and MDA levels, increased GSH and testosterone levels, ameliorated structural organization and increased claudin-11 patches number. We demonstrated a protective effect of MI, a minor role of Se and an evident positive role of the association between MI and Se on Cd-induced damages of the testis. MI alone or associated with Se might protect testes in subjects exposed to toxicants, at least to those with behavior similar to Cd.

Infliximab abrogates cadmium-induced testicular damage and spermiotoxicity via enhancement of steroidogenesis and suppression of inflammation and apoptosis mediators

Cadmium(Cd) is a serious environmental and occupational contaminant that represents a serious health hazard to humans and other animals. Reproductive health problems have been reported in men exposed to Cd. Testicular damage is one of the deleterious effects due to Cd exposure. Cd-induced testicular toxicity is mediated through oxidative stress, inflammation, testosterone inhibition and apoptosis. Thus, the present study was performed to assess the possible protective role of infliximab (IFX), anti-TNFα agent, against Cd-induced testicular damage and spermiotoxicity in rats. The rats were randomly allotted into six experimental groups: control, Cd sulphate treated, Cd sulphate treated with infliximab (5 mg/kg), Cd sulphate with infliximab (7 mg/kg), infliximab alone (5 mg/kg), and infliximab alone (7 mg/kg). The control group received saline. To induce testicular damage, Cd sulphate (1.5 mg/100 gm body weight/day) was dissolved in normal saline and orally administrated for 3 consecutive weeks. The rats in infliximab-treated groups were given a weekly dose of 5 mg/kg/week or 7 mg/kg/week of infliximab intraperitoneally. In the current study Cd exposure reduced sperm count, markers of testicular function, sperm motility as well as gene expression of testicular 3β-HSD and 17β-HSD and serum testosterone level. Additionally, it increased testicular oxidative stress, inflammatory and apoptotic markers. The histopathologic studies supported the biochemical findings. Treatment with infliximab significantly attenuated Cd-induced injury verified by the restoration of testicular architecture, enhancement of steroidogenesis, preservation of spermatogenesis, modulation of the inflammatory reaction along with suppression of oxidative stress and apoptosis. It was concluded that infliximab, through its antioxidant, anti-inflammatory and anti-apoptotic effects, represents a potential therapeutic option to protect the testicular tissue from the detrimental effects of Cd.

Protective Effect of Ganoderma Triterpenoids on Cadmium-Induced Testicular Toxicity in Chickens.

Studies have shown that cadmium can cause chicken testicular damage, but a protective effect of Ganoderma triterpenoids on cadmium-induced testicular damage in chickens has not yet been reported. The present study was designed to research the protective effect of Ganoderma triterpenoids on cadmium-induced testicular damage in chicken. Eighty healthy 7-day-old Hyline egg laying chickens were randomly divided into four groups with 20 in each group. The control group was fed with normal full-fodder, the model group was fed with normal full-fodder with 140mg/kg of CdCl2, the Ganoderma triterpenoid treatment group was fed with a full-fodder diet containing 140mg/kg of CdCl2 and 0.5mL of Ganoderma triterpenoid solution (20mg/mL), and the Ganoderma triterpenoid group was fed normal full-fodder and 0.5mL of Ganoderma triterpenoid solution (20mg/mL) gavage. The chickens were euthanized at 20, 40, and 60days, respectively, and the testes were harvested. The changes of cadmium contents, the antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px)), peroxide (malondialdehyde (MDA)), inflammatory factors (interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α)), and apoptosis-related proteins (Bax, Bcl-2, and Caspase-3) were detected. The pathological sections of the testes were made at the same time. The results suggested that Ganoderma triterpenoids could reduce the accumulation of cadmium in testis tissue; reduce the content of IL-1β, IL-6, and TNF-α in cadmium poisoning testis; significantly increase the activity of SOD and GSH-Px; decrease the content of MDA; regulate the expression of Bax, Caspase-3, and Bcl-2; and reduce the damage of testicular tissue. The results showed that Ganoderma triterpenoids have a protective effect on cadmium-induced testicular injury in chicken.

Mimosa pudica Protects the Testes Against Cadmium-Induced Inflammation and Oligospermia: Potential Benefits in Treatment of Heavy Metal Toxicity

Cadmium is a known environmental and industrial pollutant with an enormous tissue disrupting potential. Mimosa pudica (M. pudica) is a creeping annual or perennial herb known to possess anti asthmatic, anti-epileptic, anti-tumour, anti-fertility, aphrodisiac, analgesic, anti-depressant, sedative, emetic properties and a strong radical scavenging activity. This research was aimed at investigating the ameliorative effects of M. pudica on cadmium-induced testicular damage in adult male Sprague Dawley rats. Twenty adult Sprague Dawley rats were employed in the study. They were divided into 4 groups (A–D) of 5 rats each, and toxicity was induced by administering 0.4 mg/ml cadmium chloride through drinking water to groups B–D for 21days. M. pudica extract was administered orally at 250 and 500 mg/kg to groups C and D. Animals in Groups C and D showed remarkable histological improvements in testicular tissue and markedly reduced damages when compared with group B.The active sperm motility of group B (6.00 ± 1.00%) was significantly (p = 0.0001) decreased compared to that of the groups A (15.00 ± 0.00%)) and C (13.00 ± 1.22%). Sperm count analysis of group B (1.36 ± 0.28 × 106/cc), C (4.18 ± 0.81 × 106/cc) and D (2.54 ± 1.13 × 106/cc) were significantly lower (p = <0.05) when compared with group A (12.78 ± 0.92 × 106/cc), respectively. Sperm morphology of group A (70.00 ± 3.16%), B (66.00 ± 2.50), C (74.00 ± 2.45%) and D (64.00 ± 2.45%) recorded no significant difference. This study demonstrates that M. pudica has potential protective and restorative properties on the histoarchitecture of the testes of cadmium-treated rats.

Cadmium-induced testicular damage is associated with mineral imbalance, increased antioxidant enzymes activity and protein oxidation in rats

AimsCurrently, the spectrum of pathological manifestations associated with cadmium-induced testicular toxicity is poorly understood. Thus, we investigated the impact of cadmium (Cd) exposure on testicular mineral bioavailability, activity of antioxidant enzymes, testicular structure and germ cells ultrastructure Main methodsCadmium chloride was administered in a single dose to thirty rats equally randomized into five groups: Saline, 0.9% NaCl; Cd1 – Cd4, 0.67, 0.74, 0.86 and 1.1mgCd/kg. Seven days after Cd exposure, animals were euthanized and testes were collected for biochemical analysis, as well as light, scanning and transmission electron microscopy. Key findingsCadmium exposure induced dose-dependent testicular toxicity. Tubular and intertubular compartments were targets of Cd and calcium (Ca) deposits, marked structural and ultrastructural pathologic remodeling, and a reduced distribution of iron, selenium, magnesium, copper, zinc and total protein. Despite upregulation in antioxidant enzyme activities (i.e. catalase [CAT] and superoxide dismutase [SOD]), morphologic and molecular testis damage such as protein oxidation was not prevented, especially with higher doses of Cd. As non-degenerated tissue areas also presented Ca deposits, Ca imbalance was not only a consequence but also a cause of Cd-induced testis toxicity and germ cell death SignificanceTaken together, our findings indicated that Cd exposition induced dose-dependent testicular dystrophic calcification, which was associated with increased antioxidant enzymes activity and protein oxidation, mineral imbalance, germ cell calcification and death in rats. Although increased CAT and SOD activity represents a counter-regulatory reaction to cadmium-induced toxicity, this reaction is insufficient to prevent testicular pathological remodeling.

Sulforaphane Prevents Testicular Damage in Kunming Mice Exposed to Cadmium via Activation of Nrf2/ARE Signaling Pathways.

Sulforaphane (SFN) is a natural and highly effective antioxidant. Studies suggest that SFN protects cells and tissues against cadmium (Cd) toxicity. This study investigated the protective effect of SFN against oxidative damage in the testes of Kunming mice exposed to cadmium, and explored the possible molecular mechanisms involved. Cadmium greatly reduced the serum testosterone levels in mice, reduced sperm motility, total sperm count, and increased the sperm deformity rate. Cadmium also reduces superoxide dismutase (T-SOD) and glutathione (GSH) levels and increases malondialdehyde (MDA) concentrations. SFN intervention improved sperm quality, serum testosterone, and antioxidant levels. Both mRNA and protein expression of mouse testicular nuclear factor-erythroid 2-related factor 2 (Nrf2) was reduced in cadmium-treated group. Furthermore, the downstream genes of Nrf2, glutathione peroxidase (GSH-Px), γ-glutamyl cysteine synthetase (γ-GCS), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) were also decreased in cadmium-treated group. SFN intervention increases the expression of these genes. Sulforaphane prevents cadmium-induced testicular damage, probably via activation of Nrf2/ARE signaling.

Ameliorative effect of propolis on the cadmium-induced reproductive toxicity in male albino rats

Propolis is a potent antioxidant and a free radical scavenger. The present study aimed to investigate protective effects of propolis extract on cadmium-induced testicular damage, apoptosis, HIF-1α expression and toxicity in rat's testis tissue.A total of 32 male rats were equally divided into four study groups namely, control, Cd (1mg/kg/day), Cd+propolis (50mg/kg/day) and propolis. The rats were decapitated under ketamine anesthesia and their testes tissues were removed. Serum testosterone, tissue malondialdehyde and HIF-1α levels, HIF-1α expression, apoptosis and histopathological damage scores were then compared.In the Cd group, the diameters of seminiferous tubules, tubular biopsy score of Johnsen and serum testosterone levels were decreased compared control group, but tissue HIF-1α and tissue MDA levels was higher than control group. The immunoreactivity of HIF-1α and the number of apoptotic cells were increased in Cd group. Furthermore, the propolis treated group showed an improved histological appearance in the Cd group.Thus, the results suggest that propolis acts as a potent protective agent against Cd-induced testicular toxicity in rats.