Protective effect of chlorella vulgaris on testicular damage, sperm parameters, androgen production, apoptosis and oxidative stress index in male rats following doxorubicin administration.

Doxorubicin (DOX) is a chemotherapy agent associated with adverse effects on male reproductive health. Chlorella vulgaris (ChV) is a potent natural antioxidant with promising applications in maintaining health and preventing oxidative stress-related diseases. The present study aimed to investigate the protective effect of ChV on DOX-induced testicular toxicity. Twenty-five Wistar rats (230 ± 20g) were randomly assigned to five groups (n = 5), including the control group, sham group (received normal saline by oral gavage daily and intraperitoneally (IP) once a week), DOX group (3mg/kg; once a week; IP), ChV group (300mg/kg/day; by oral gavage), and DOX (3mg/kg; once a week; IP) + ChV (300mg/kg/day; by oral gavage) group. After 8 weeks of treatment, the rats were euthanized and serum testosterone level, testes histomorphometry, gonadosomatic index (GSI), apoptotic gene expression, oxidative stress index, and sperm parameters were assessed. The results showed that DOX led to a significant decrease in histological indexes, testosterone level, GSI, sperm parameters, and Bcl-2 gene expression and increased expression of P-53 and Bax genes, and oxidative stress markers (P<0.05). The administration of ChV in the DOX+ChV group significantly improved testosterone levels, sperm parameters, testicular tissue apoptosis, antioxidant enzymes, and structural integrity of the testes (P<0.05). The findings suggest that the co-administration of ChV can be a promising therapeutic agent to reduce the adverse effects of DOX on male reproductive performance.

Dimethyl itaconate mitigates histological distortions, inflammation, and oxidative stress in the rat model of polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is the most common cause of anovulation and infertility in women. Inflammation and oxidative stress are considered to be the causes of ovarian dysfunction in PCOS. Dimethyl itaconate, as a macrophage-derived immunometabolite, has anti-inflammatory and antioxidative properties, but limited data are available about its effect on female reproductive dysfunctions. The present study aimed to determine the effects of dimethyl itaconate, a cell-permeable derivative of itaconate, on the histological changes, oxidative stress, and inflammation in the ovaries of PCOS rats. In this experimental study, 48 mature female Wistar rats (160-180 g) were randomly divided into the six groups including control, PCOS, PCOS+DMI, PCOS+ metformin, control DMI and control metformin. Following PCOS induction by using testosterone enanthate (1 mg/100 g/day for 35 days), the animals were treated with DMI (50 mg/kg) or metformin (300 mg/kg) for 30 days. At the end of the experimental period, the insulin resistance markers (serum insulin and glucose concentrations, and the homeostasis model assessment of basal insulin resistance (HOMA-IR), oxidative stress index (OSI), and inflammatory cytokines were measured. The process of Folliculogenesis was evaluated by histological examination of the ovary. The results showed that DMI improved insulin resistance and decreased TNF- and IL-1ß levels and OSI in the ovarian tissue of rats following androgen-induced PCOS. It also improved steroidogenesis and Folliculogenesis by reducing cystic follicles and ovarian tissue structure. Results indicated that DMI may be a potential candidate to ameliorate PCOS adverse effects by reducing insulin resistance, inflammation, and oxidative stress and restoring ovarian Folliculogenesis.

Effects of chemical and green nano-zinc oxide on histological changes, oxidative stress, and apoptosis in rat kidney associated with cisplatin

Abstract Cisplatin (CP) is used to treat various tumors. A main restriction of cisplatin is nephrotoxicity. This study aimed to evaluate the protective effects of ZnONPs on cisplatin-induced oxidative stress and rat kidney tissue damage. Eighty adult male Wistar rats (250g-270g) were divided into ten groups: Control (CON), Sham (SH), Bulk ZnO (BZnO), Chemical ZnONPs (ChZnONPs), Green ZnONPs (GrZnONPs), Cisplatin (CP), Cisplatin+BulkZnO (CP+BZnO), Cisplatin+Green ZnONPs (CP+GrZnONPs), Cisplatin+Chemical ZnONPs (CP+ChZnONPs), Cisplatin+Explant (CP+EX). CP was i.p administered 5mg/kg/week and BZnO, ChZnONPs and GrZnONPs were i.p administered at a dose of 5mg/kg/day. After 30 days of the treatment, the expression of apoptosis/anti apoptosis related genes oxidant/antioxidant factors and histological changes in the were studied. The CP-treated group showed a decrease in body weight, while the Co-administration of ZGNPs to CP-treated rats showed a significant increase compared to the CP group. The results showed that the increased mRNA level of bax, MDA and the decreased mRNA level of bcl2, SOD and CAT activities in kidney of CP group were improved when animals were treated with ZnO NPs. Our results showed that GrZnONPs, ChZnONPs and BZnO had the potential to protect against oxidative stress and cisplatin-induced neurotoxicity that this protective effect was more evident in GrZnONPs.

Protective effects of Aloe vera gel on cisplatin-induced oxidative stress, apoptosis and neurons structure in rat hippocampus.

Cisplatin (CP) as an important chemotherapeutic drug is used for the treatment of various malignancies; but it has some side effects on central nervous system, in particular hippocampus. The present study was aimed to determine the protective effects of Aloe vera (AV) gel on CP-induced oxidative stress, apoptosis and neurons structure changes in the hippocampus of rats. Forty-eight rats were divided into six groups including control, CP (5.00 mg kg-1 per week; intraperitoneally), CP + AV (400 mg kg-1 per day; orally), CP + metformin (200 mg kg-1 per day; orally), AV (400 mg kg-1 per day; orally) and metformin (200 mg kg-1 per day; orally). At the end of treatment, brain samples were obtained for analysis of apoptotic genes expression and anti-oxidant markers as well as histological study. The results showed that CP caused an increase in malondialdehyde level and a decrease in glutathione peroxidase, superoxide dismutase and catalase levels in CP group compared to control. The AV gel could diminish oxidative stress in the hippocampus of CP group and it resulted in down-regulation of Bax, caspase-3 and caspase-8 and up-regulation of Bcl-2 in CP group. It could ameliorate degenerative changes in hippocampus after exposure to CP. Our results showed that AV gel ameliorated oxidative stress, apoptosis and neuronal loss in the hippocampus of rats under CP treatment.

Chemical and Green ZnO nanoparticles ameliorated adverse effects of cisplatin on histological structure, antioxidant defense system and neurotrophins expression in rat hippocampus.

Cisplatin (CP) is a chemotherapy agent used in the treatment of cancer, but it has various side effects, in particular, neurotoxicity. Zinc oxide nanoparticles (ZnO NPs) are a potent antioxidant. However, there is limited knowledge about the protective effects of ZnO NPs against CP-induced hippocampal toxicity. The present study aimed to explore the potential protective effects of ZnO NPs against CP-induced oxidative stress, loss of neurotrophins support, and tissue damage in the hippocampus of the rats. Eighty adult male Wistar rats were dividing into ten groups including: control (Con), sham, ZnO Bulk (ZnB), chemical ZnO NPs (ChZnO NPs), Green ZnO NPs (GrZnO NPs), CP, CP + ZnB, CP + ChZnO NPs, CP + GrZnO NPs and CP + AE. CP was administrated (5 mg/kg/weekly) for four weeks, and animals were treated simultaneously with different forms of ZnO (5 mg/kg/day). At the end of the experiment, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), malondialdehyde (MDA), changes of reduced glutathione (GSH), oxidized glutathione (GSSG) and GSH/GSSG ratio, histological changes, expression of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) genes were assessed in the hippocampus. The results revealed that a decrease in BDNF and NGF mRNA expression, GSH concentration and GSH/GSSG ratio, increasing of GSSG and MDA levels, and neuronal loss in the CP-treated rats were reversed following the administration of different forms of ZnO, especially Gr ZnO NPs and ch ZnO NPs. Co-administration of ZnO NPs to CP-treated rats restored the suppressive effects of CP on activities of antioxidant enzymes (SOD, GPX, CAT). The results showed that in most of the evaluated factors, Gr ZnO NPs showed a greater protective effect than other forms of ZnO. The results suggest that ZnO NPs, in particular Green ZnO NPs (GrZnO NPs) had more potential protective effects against CP-induced oxidative stress, inadequate support neurotrophin and tissue damage in rat hippocampus.

Attenuation of heat stress-induced spermatogenesis complications by betaine in mice.

High temperatures can induce oxidative stress, impairment of spermatogenesis, and reduction of sperm quality and quantity concomitant with transient periods of partial or complete infertility in male mammals. Promising beneficial effects of betaine supplementation on the epididymal spermatozoa have been reported in experimental studies; however, its effects on testicular heat stress (HS)-induced impairment have yet to be determined. In the present study, betaine (Bet) was orally administrated (250 mg/kg day) during a 14-day period, before (Bet + HS group) or after (HS + Bet group) induction of testicular HS in 7-9 week-old male mice. HS was induced by testicular immersion in water at 42 °C in stress groups. Epididymal spermatozoa and testes were collected at days 14 and 28 after HS induction in order to analyze sperm characteristics, testicular oxidative status, and histological changes. Our studies showed that HS reduced testicular weight, the quality and quantity of epididymal spermatozoa, and impaired maturation of germinal cells. The levels of MDA, catalase, SOD, and GPX were increased in the testes of HS-induced mice (P < 0.01). Although betaine treatment before and after exposure to HS enhanced antioxidant defense (P < 0.05) and accelerated germinal epithelium regeneration, its effects on the characteristics of epididymal spermatozoa were scarce. On the other hand, in the absence of heat stress, quality and quantity of epididymal spermatozoa were improved following 14 days of betaine consumption. Our study revealed the beneficial effect of betaine on HS-induced complications of spermatogenesis, as well as its potency to improve epididymal spermatozoa in intact mice.