The protective effect of aqueous extract of Stevia rebaudiana against tartrazine toxicity in male Wistar rat.

Tartrazine is a yellow colouring agent that is commonly used in foods; however, high dosages of Tartrazine affect fertility and create oxidative stress by generating free radicals. A plant species known as Stevia rebaudiana has natural antioxidants that show promise for protecting testicular tissue. Consequently, this study was intended to examine the ameliorative effect of the aqueous extract of S. rebaudiana (Stevia) on the fertility of male Wistar rats induced by the daily oral intake of Tartrazine. Utilizing gas chromatography-mass spectrometry, phytochemical identification was accomplished for Stevia extract. Study groups were separated into several groups: the first group (the control) got distilled water for up to 56 days; the Stevia group (1000 mg/kg), the Tartrazine group (300 mg/kg) and the Stevia and Tartrazine group (the group was given Tartrazine after 1 h of Stevia extract intake). Also, the oxidative damage in testicular tissues was assessed by measuring the levels of malondialdehyde (MDA) and antioxidants (catalase [CAT], superoxide dismutase [SOD] and glutathione reductase [GSH]). Further, histological alterations were examined. In addition, cyclic AMP-responsive element modulator (Crem) gene expression levels and their relative proteins were measured in the testicular tissues using quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assays, respectively. Sperm analysis and testosterone concentration were also performed. SPSS version 25 was used for the analysis of results while (p < .05) was regarded as significant. Compared with the control group, the results demonstrated that Tartrazine caused a significant reduction (p < .05) in the testosterone hormone level (0.70 ± 0.21) and the Crem protein quantity (1.21 ± 0.23) in the treated Tartrazine group. Also, it had a significant decrease (p < .05) in sperm motility, viability, count and antioxidant levels. Moreover, there was a significant increase (p < .05) in sperm abnormalities, MDA level (7.40 ± 1.10), kidney and liver function parameters, and DNA degradation in the treated Tartrazine group compared with the control group. On the contrary, the Stevia extract intake enhanced the testosterone (2.50 ± 0.60), antioxidants and Crem protein levels (2.33 ± 0.10) with an improvement in sperm quality in the Stevia and Tartrazine-treated group compared with the Tartrazine group. Stevia also caused a significant decrease (p < .05) in the MDA level (3.20 ± 0.20), and sperm abnormalities with an enhancement of the liver and kidney function parameters in the Stevia and Tartrazine-treated group compared to the Tartrazine group. Stevia administration has a protective effect on the testicular tissues and sperm quality against toxicity induced by Tartrazine exposure, so it will be a good antioxidant drug to be administered daily before daily administration of Tartrazine.

Induction of apoptosis, oxidative stress, hormonal, and histological alterations in the reproductive system of thiamethoxam-exposed female rats.

The present study aimed to investigate the oral toxic effects of 1/10 LD50 and 1/5 LD50 of thiamethoxam (TMX), a neonicotinoid insecticide, on the reproductive system of female Wistar rats. Thirty female rats were divided into three groups and supplied orally with either; saline solution, 1/10 LD50 of TMX (156 mg/kg) or 1/5 LD50 of TMX (312 mg/kg). The daily administration was extended for 30 days. Investigating the parameters of oxidative stress, hormonal levels, histopathological alterations, and the apoptotic markers (P53, BAX, BCL-2, and caspase-3) was performed in the uterus and ovary of rats. Results showed significant changes in the body weight gain, and relative weight of the left and right ovaries and uterus. Moreover, luteinizing hormone (LH), estradiol (ED), and progesterone (PG) serum levels were not significantly altered following TMX oral administration. The level of follicle-stimulating hormone in the TMX-exposed group (156 mg/kg) was significantly increased; however, a significant decrease was observed in TMX-exposed animals (312 mg/kg). TMX induced significant oxidative stress in exposed groups by reducing the activities of superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT), and elevating malondialdehyde (MDA) levels. Following hematoxylin and eosin staining, the microscopic examination revealed deteriorated luteal cells with vacuolation in the corpus luteum, a follicle containing a degenerated oocyte and degeneration/necrosis of the circular muscle layer with a high rate of apoptotic cells in TMX-exposed animals. TMX induced transcriptional alterations in apoptosis-related genes shifting towards the activation of the intrinsic apoptotic pathway. Collectively, results suggest the toxic effect of the TMX on the reproductive health of female Wistar rats.

Ameliorative effects of nano Moringa on fluoride-induced testicular damage via down regulation of the StAR gene and altered steroid hormones.

Fluoride is a common environmental contaminant that has harmful effects on human health when it is present in high concentrations. Fluoride enters the bloodstream after being absorbed by the gastrointestinal system when fluoride-contaminated groundwater is consumed by people. The aim of the present study was to determine whether polyphenol-rich nano Moringa oleifera (NMO) could protect rat testicles from sodium fluoride (NaF) damage by evaluating sperm quality, sex hormones, testicular oxidative status, histopathology, and StAR gene expression. Twenty-eight adult Wistar rats were divided equally and randomly into four groups: group one received distilled water; group two received NMO at a dosage of 250 mg/kg/body weight; group three received NaF at a dosage of 10 mg/kg/body weight; and group four received NaF and NMO. The rats were orally administrated daily for a duration of eight weeks. The study's findings demonstrated that, in comparison to rats exposed to NaF alone, co-administration of NMO and NaF enhanced sperm motility and viability, decreased sperm morphological changes, restored the balance between oxidant and antioxidant status, improved testosterone and dehydroepiandrosterone, improved testicular histology, raised the Johnson score, and upregulated the StAR gene in testicular tissue. These findings show that NMO is promise as a prophylactic medication against sodium fluoride-induced testicular damage because administration of NMO had no adverse effects and enhanced reproductive health.

Assessment of the potential toxic effect of magnetite nanoparticles on the male reproductive system based on immunological and molecular studies.

Magnetite nanoparticles (MNPs) are the most conventional type of iron oxide nanoparticles used in the food industrial processes, removal of heavy metals, and biomedical applications in vivo or in vitro. Until now, there is no sufficient information that can confirm its effect on the body's immune system and reproductive health in males. The purpose of this research is to estimate the immunotoxic and reproductive toxic effects of MNPs in male rats. This study included 36 adult male albino rats divided into three groups. The experimental groups were intraperitoneally injected with MNPs at doses of 5 and 10 mg/kg body weight 3 times/week for 60 days, while the control group was injected with saline solution. MNPs caused a significant decrease in the body weight change of the high-treated group. MNPs produced changes in the lymphocyte proliferation rate which referred to a significant immunotoxic effect measured by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide reduction method. The testicular tissue of male-treated rats showed some moderate and severe degenerative changes. The sperm parameters of count, motility, and viability were significantly decreased. Sperm morphological abnormalities were detected in all treated animals. MNPs produced a significant decrease in testosterone levels, increased the level of malondialdehyde, impaired the activity of the antioxidant enzymes and induced testicular DNA damage. In conclusion, MNPs affected the normal immune state in male rats and facilitated the generation of reactive oxygen species subsequently triggering testicular oxidative stress damages. All these consequences had a negative impact on male reproductive health.

Impact of maternal desvenlafaxine exposure on brain development in pregnant albino rats and their fetuses.

Depression during pregnancy adversely affects fetal development. Desvenlafaxine drug is used for the treatment of gestational depression. In light of the well-established role of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in regulating neurogenesis and neural survival, the role of S100b in nerve cell energetic metabolism, differentiation of neurons and glial cells, an aberrant increase in NGF, BDNF and S100b expression in the fetal brain may contribute to desvenlafaxine cognitive disorders by altering brain development. This study is trying to determine the effect of desvenlafaxine on brain development. Thirty timed pregnant rats (from the 5th to the 20th day) were divided into three groups: control, low dose (5.14 mg/kg/day) and high dose (10.28 mg/kg/day) of desvenlafaxine where all animals received the corresponding doses by gavage. Maternal and fetal brain samples were fixed for histological, immunohistochemical (IHC) study of NGF and evaluated for BDNF and S100b genes expression. Desvenlafaxine induced some of the histopathological alterations in maternal and fetal rat brains. Moreover, IHC analysis of maternal and fetal rat brains showed that groups treated with desvenlafaxine demonstrated a significant increase of NGF protein immunoreactivity compared with that in the controls. Gene expression results revealed upregulation of messenger RNA BDNF and S100B expression. According to developmental changes in the brain, desvenlafaxine affects neonatal growth during pregnancy, which may lead to delay of brain development. So, it is essential to survey the roles of antidepressant drugs on neonatal development during pregnancy.