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Impaired spermatogenesis and male infertility are common consequences of chemotherapy drugs used in patients with testicular cancer. The present study investigated the effects of sodium alginate (NaAL) on testicular toxicity caused by bleomycin, etoposide, and cisplatin (BEP). Rats in group 1 received normal saline, while groups 2 and 3 were treated with 25 and 50 mg/kg of NaAL, respectively. Group 4 was treated with a 21-day cycle of BEP (0.5 mg/kg bleomycin, 5 mg/kg etoposide, and 1 mg/kg cisplatin), and groups 5 and 6 received BEP regimen plus 25 and 50 mg/kg of NaAL, respectively. Then, sperm parameters, testosterone levels, testicular histopathology and stereological parameters, testicular levels of malondialdehyde (MDA), nitric oxide (NO), and total antioxidant capacity (TAC), and the expression of apoptosis-associated genes including Bcl2, Bax, Caspase3, p53, and TNF-α were evaluated. Our findings revealed that NaAL improved sperm parameters, testosterone levels, histopathology, and stereology parameters in BEP-administrated rats. NaAL also improved testis antioxidant status by enhancing TAC and ameliorating MDA and NO. Further, modifications to the expression of Bcl2, Bax, Caspase3, p53, and TNF-α suggested that NaAL alleviated BEP-induced apoptosis and inflammation. Collectively, NaAL protects rats' testes against BEP-evoked toxicity damage through the modulation of nitro-oxidative stress, apoptosis, and inflammation. [ABSTRACT FROM AUTHOR]

There is a growing concern that antidepressant drugs impair sexual function and adversely impact spermatogenesis and male fertility. Vitamin C is a natural antioxidant that plays a vital role in the male reproductive system. The present study investigated the ameliorating potential of vitamin C against citalopram (CTL)‐evoked testicular toxicity and spermatogenesis impairment in mice. Mice were randomly divided into six groups: control, CTL, vitamin C 100, vitamin C 200, CTL plus vitamin C 100, and CTL plus vitamin C 200. Adult male mice were intraperitoneally (ip) injected with 10 mg/kg of CTL for 35 days with or without vitamin C. At the end of the study, body and testes weight, sperm parameters, histopathology of testes, testosterone level, testicular levels of malondialdehyde (MDA), nitric oxide (NO), total antioxidant capacity (TAC), and apoptosis (TUNEL assay) were evaluated. Our findings revealed that vitamin C restored spermatogenesis by improving sperm count, motility, viability, morphology, and chromatin integrity. Testosterone levels and testes histopathology were significantly improved in the vitamin C‐administrated groups. Furthermore, vitamin C administration markedly alleviated CTL‐induced nitro‐oxidative damage, enhancing TAC levels, and reducing NO and MDA levels. Whilst CTL therapy induced a significant increase in the number of TUNEL‐positive cells compared to the control, the administration of vitamin C significantly prevented the apoptotic effects of CTL. Together, vitamin C therapy protects against CTL‐induced testicular damage via mitigating nitro‐oxidative stress and apoptosis, which provides evidence for vitamin C as a beneficial therapy against antidepressant drug‐associated reproductive toxicity and male sub/infertility. [ABSTRACT FROM AUTHOR]

L‐Proline is a natural anti‐oxidative and osmoprotectant agent, playing a versatile role in cell metabolism and physiology. The present study aimed to explore the antioxidant effects of L‐Proline on human sperm function during incubation. Thirty healthy, normozoospermic men (27–40 years) were enrolled. Sperm samples were incubated in an unsupplemented sperm medium (control group), or supplemented with L‐Proline (1, 2 and 4 mmol/L) to evaluate its effect during 0, 1, 4 and 24 h of incubation. Sperm were assessed in terms of motility, viability, morphology, chromatin and DNA integrity. Moreover, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and total antioxidant capacity (TAC) were determined in the sperm medium. The results indicated that 2 mmol/L of L‐Proline significantly improved the maintenance of sperm motility, viability, normal morphology, chromatin and DNA integrity, and TAC levels compared to the control group during 24 h of incubation (p < 0.05). However, 1 and 4 mmol/L of L‐Proline could not significantly preserve sperm parameters, chromatin quality, and antioxidant status during different incubation times compared to the control group (p > 0.05). Collectively, the inclusion of L‐Proline (2 mmol/L) in the human sperm medium maintains sperm parameters and chromatin quality probably by modulating the oxidative status. [ABSTRACT FROM AUTHOR]

Sperm cryopreservation as a routine technique in assisted reproductive technique (ART) laboratories has detrimental effects on spermatozoa. Various methods have been introduced to improve it. The aim of this research was to evaluate the effects of L‐proline supplementation in cryopreservation medium on normozoospermic semen samples. A total of 30 semen samples were collected from normozoospermic men. Cryopreservation media were supplemented with different concentrations of L‐proline (0, 1, 2 and 4 mmol/L). The semen samples were cryopreserved. After thawing, sperm parameters and chromatin integrity (aniline blue (AB), toluidine blue (TB), sperm chromatin dispersion test (SCD) and chromomycin A3 (CMA3)), reactive oxygen species (ROS), and total antioxidant capacity (TAC) and malondialdehyde (MDA) levels were evaluated. A total of 4 mmol/L L‐proline significantly improved progressive motility and viability (p < 0.05). MDA and ROS levels significantly diminished in samples were cryopreserved by 4 mmol/L L‐proline supplemented cryopreservation media (p < 0.001). Also, it significantly increased TAC level. Also, chromatin damages (AB, TB and CMA3) significantly improved in samples were cryopreserved by 4 mmol/L L‐proline supplemented cryopreservation media (p < 0.05). The results support that the usage of L‐proline supplemented cryopreservation media to improve sperm quality after cryopreservation. [ABSTRACT FROM AUTHOR]

Cisplatin can lead to infertility due to its negative impact on the uterus and ovaries. This study aimed to explore the effects of Inositol and vitamin C on cisplatin-induced infertility. Forty-eight adult female Wistar rats were divided into eight groups (N = 6) and orally treated for 21 days. The treatments were as follows: negative control (saline), positive control (saline and cisplatin injected into the abdomen on day 15), T1–T3: rats given vitamin C (150 mg/kg), Inositol (420 mg/kg), and vitamin C + Inositol, respectively, along with cisplatin injected into the abdomen on day 15, T4–T6: rats given only vitamin C, Inositol, and vitamin C + Inositol, respectively. Vitamin C and Inositol enhanced cisplatin-induced histopathological improvements in the uterus and ovaries, raising progesterone and estradiol serum levels. Furthermore, the supplements enhanced ESR1 gene expression in the uterus and ovary, reducing uterine and ovarian apoptosis caused by cisplatin through modulation of caspase 3, 8, and Bcl-2 gene levels. These substances decreased ovarian and uterine malondialdehyde levels, boosted total antioxidant capacity and superoxide dismutase, and alleviated oxidative stress. The findings reveal that vitamin C and Inositol shield against cisplatin-related infertility by reducing oxidative stress and apoptosis in the uterus and ovaries. • This study focuses on ovarian and uterine toxicity induced by cisplatin in rats. • Histopathology of the uterus and ovaries including follicle count was investigated. • Oxidative stress indices and apoptosis markers, were also investigated. • The protective effects of inositol and vitamin C is well indicated. [ABSTRACT FROM AUTHOR]

Citalopram is the most potent selective serotonin reuptake inhibitor, commonly prescribed as an antidepressant, which can cause sexual dysfunction. Melatonin is a natural, highly effective antioxidant playing a pivotal role in the male reproductive system. The present study aimed to explore the ameliorating potential of melatonin on citalopram-evoked testicular toxicity and injury in mice. In this regard, mice were randomly divided into six groups: control, citalopram, melatonin 10 mg/kg, melatonin 20 mg/kg, melatonin 10 mg/kg plus citalopram, and melatonin 20 mg/kg plus citalopram. Adult male mice were intraperitoneally (i.p.) injected with 10 mg/kg of citalopram for 35 days with or without melatonin. At the end of the study, sperm parameters, testosterone level, testicular levels of malondialdehyde (MDA), nitric oxide (NO), total antioxidant capacity (TAC), and apoptosis (Tunel essay) were evaluated. Our findings revealed that melatonin restored spermatogenesis by improving sperm count, motility, viability, morphology, and chromatin integrity. Testosterone levels and the histopathology of the testes were markedly improved in the melatonin-administrated groups. Furthermore, citalopram administration significantly increased oxidative stress; however, melatonin restored antioxidant status by enhancing TAC levels and decreasing NO and MAD levels. More notably, citalopram therapy induced a significant increase in the number of Tunel-positive cells, while melatonin administration significantly mitigated the apoptotic impacts of citalopram. Together, melatonin therapy provides protection against citalopram-induced testicular damage via modulating nitro-oxidative stress and apoptosis, which provides evidence for melatonin as a promising treatment against antidepressant drug-associated reproductive toxicity and male sub/infertility. • Melatonin attenuates citalopram-induced testicular toxicity and sperm damage. • Melatonin regulates nitro-oxidative stress and apoptosis in testes. • The beneficial effects of melatonin were not dose-dependent. • Melatonin could alleviate antidepressant-associated reproductive toxicity. [ABSTRACT FROM AUTHOR]

There is growing concern that some cytotoxic regimens for cancer adversely affect spermatogenesis and male fertility. Increasing evidence demonstrated that melatonin has beneficial impacts on reproductive processes; however, whether melatonin can protect against bleomycin, etoposide, and cisplatin (BEP) chemotherapy regimen-induced testicular toxicity, remains obscure. The present study aimed to explore the effect of melatonin on BEP-evoked testicular injury in rats. Adult male Wistar rats (n = 10/group) were intraperitoneally (i.p.) injected with one cycle of 21 days of 0.33 therapeutically relevant dose levels of BEP (.5 mg/kg bleomycin, 5 mg/kg etoposide, and 1 mg/kg cisplatin) with or without melatonin. At the end of the study, sperm parameters, testosterone level, stereology of testes, testicular levels of malondialdehyde (MDA), nitric oxide (NO), and total antioxidant capacity (TAC), the expression of apoptosis-associated genes such as Bcl2 , Bax , Caspase-3 , p53 , and TNF-α (Real-time PCR and Immunohistochemistry) were evaluated. Our findings showed that melatonin restored spermatogenesis by improving sperm count, motility, viability, and morphology. Testosterone level, histopathology, and stereology of testes were significantly improved in melatonin-administrated groups. Furthermore, melatonin recovered the oxidative status of the testes through elevating TAC and ameliorating MDA and NO levels. More importantly, melatonin therapy suppressed BEP-evoked apoptosis by modulating Bcl-2 , Bax , Caspase-3 , p53 , and TNF-α expression in testes. In conclusion, melatonin protects the testes against BEP-induced testicular damage by attenuating nitro-oxidative stress, apoptosis, and inflammation, which provides evidence for melatonin as a possible clinical therapy against BEP-associated gonadotoxicity and male sub/infertility. [Display omitted] • Melatonin attenuated bleomycin, etoposide, and cisplatin (BEP) chemotherapy-induced testicular toxicity. • Melatonin's protective effect was attributed to nitro-oxidative stress, apoptosis, and inflammation regulation. • Melatonin alleviative effects were not exerted in a dose-dependent manner. • Melatonin might be a pharmacological therapeutic approach for minimizing BEP-associated male infertility. [ABSTRACT FROM AUTHOR]