Aspartame is one of the most common consumed artificial sweeteners utilized in many food products and beverages. It has been indicated that long‐term consumption of aspartame leads to reproductive toxicity but its mechanism is not well‐clear. In this study we investigated mechanism of aspartame‐induced reproductive toxicity in male mice. For this purpose, 36 NMRI mature male mice received three doses of 40, 80, and 160 mg/kg body weight of aspartame, respectively per day by gavage for 90 days and also a control group was considered which received 0.5 mL of normal saline as the same route. The results revealed that long‐term administration of aspartame at high doses significantly (P < .05) reduced gonadosomatic index, serum concentration of pituitary‐testicular axis hormones (FSH, LH, and testosterone). It also decreased sperm parameters and total antioxidant capacity, antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase), while it caused increase in nitric oxide and malondialdehyde levels in testis tissue and sperm samples. Also, it decreased attenuated testicular histomorphometric indices (tubular differentiation index, spermiogenesis index, and repopulation index), and steroidogenic foci, while increased mRNA damages and apoptosis rate, downregulated antiapoptotic (Bcl‐2) and upregulated proapoptotic (P53, BAX, and caspase‐3) mediators respectively in testis. These findings indicated that consumption of aspartame for a long period results in male reproductive toxicity by decrease in serum concentration of pituitary‐testis axis hormones and induction of oxidative stress and apoptosis in testis.

To estimate the repro‐protective effect of royal jelly (RJ) on phenylhydrazine (PHZ)‐induced anemia's detrimental effects, 24 mature mice were divided into control group (0.10 mL normal saline; intra‐peritoneally), RJ group (100 mg/kg/day; orally), experimental anemia (EA) group that received only PHZ (6 mg/100 g/48 h; intra‐peritoneally), and RJ + EA (according to the previous prescription) group. After 35 days, testicular histoarchitecture, RNA damage in germinal cells, sperm characteristics, testicular total anti‐oxidant capacity and malondialdehyde as well as serum testosterone levels, pre‐implantation embryo development and cyclin D1 and c‐myc mRNA levels at two‐cell, morula and blastocyst stages were analyzed. Spermatogenesis indices were ameliorated following RJ co‐administration. Moreover, RJ co‐treatment reduced germinal cells RNA damage, improved sperm characteristics, boosted pre‐implantation embryo development and restored androgenesis, and oxidant/anti‐oxidant status. Co‐administration of RJ also decreased mRNA levels of cyclin D1 and up‐regulated those of c‐myc in two‐cell embryos, morulas and blastocysts. The findings suggest that RJ can play a repro‐protective role in PHZ‐induced anemia in mice through anti‐oxidant defense system reinforcement and androgenesis restoration as well as cyclin D1 and c‐myc expressions regulation.

Aspartame (ASP) is probably the best known artificial sugar substitute that is used widely in food. Many experimental studies have reported the toxicity of long‐term administration of ASP in various organ tissues. However, there is little evidence available about the nature and mechanisms of the adverse effects of long‐term consumption of ASP on the cardiovascular system. This study was conducted to evaluate the possible effects of ASP on heart tissue. For this study 36 mature male mice were divided into one control group and three groups which received respectively 40 mg/kg, 80 mg/kg and 160 mg/kg ASP orally, for 90 days. ASP at the doses of 80 and 160 mg/kg increased the serum content of malondialdehyde (MDA), but decreased serum nitric oxide (NO), creatine kinase (CK) and CK‐MB, as well as blood superoxide dismutase (SOD) levels. Serum level of total anti‐oxidant capacity (TAC) in blood was also reduced in serum at the dose of 80 mg/kg. Histochemical staining, including Periodic acid‐Schiff, Masson's trichrome and Verhoeff‐van Gieson staining, indicated that ASP at doses of 80 and 160 mg/kg reduced glycogen deposition and decreased the number of collagen and elastic fibres in the cardiac tissue. The cardiac expression of pro‐apoptotic genes, including P53, Bax, Bcl‐2 and Caspase‐3, was modulated at the dose of 160 mg/kg. Moreover, transcription of Caspase‐3 was up‐regulated at the dose of 80 mg/kg. In conclusion, long‐term consumption of ASP any higher than the acceptable daily intake (40 mg/kg) appears to act by promoting oxidative stress, has the potential to alter both histopathological and biochemical parameters, and induces P53‐dependent apoptosis in cardiac tissue.

Background and objectives:Aspartame is a low-calorie synthetic sweetener that is consumed by 200 million subjects worldwide. In recent years, negative effects of aspartame have been shown on various tissues of the body. This study aimed to investigate the effects of long term consumption of aspartame at different doses on histological and histometrical structure of ventral, anterior, and dorsal lobes of prostate gland in adult mice. Methods:In this experimental study, 20 adult male mice were divided into four groups, including control group (without treatment) and groups receiving aspartame (at doses of 40, 80, and 160mg/kg/bw) by gavage for 90 days. First, the mice were euthanized, then, blood samples and tissue of the prostate lobes, were collected for histomorphological and histochemical studies. One-way ANOVA and Tukey's post hoc test, were used to compare the means in the studied groups.Results: Histological and histometrical results were indicative of a significant decrease in cell count and epithelial height of the secretory units in ventral, anterior, and dorsal lobes of the prostate in aspartame groups compared to the control group (p<0.05). Percentage of parenchyma to ventral lobe of prostate gland showed a significant decrease in aspartame groups compared to the control group (p<0.05). A significant decrease was seen in serum testosterone in dosedependent aspartame groups compared to the control group (p<0.05). Conclusion:Aspartame has a negative effect (even at low doses) on the histopathological and histometrical structure of prostate gland, especially the ventral and anterior lobes. However, further clinical studies are required to evaluate the negative effects of aspartame in human.

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Background and Objectives: Aspartame is a non-nutritive and artificial sweetener which is widely used in diet and low calorie products and also in a variety of foods, drugs and hygiene products. The present study has been conducted in order to evaluation of the effects of aspartame on ovaries in female mice. Methods: In this experimental study, 36 adult female mice were randomly divided into four groups of nine each. For three groups aspartame was administered orally with the doses of 40, 80 and 160 mg/kg.BW respectively, and one group as the control group received normal saline for 91 days by gavage. Also a control group was considered. 24 hours after the last treatment, ovarian tissue and blood samples were collected and used for biochemical, histomorphological, histomorphometric, histochemical and gene expression studies. The obtained data were analyzed using One-Way Analysis of Variance (ANOVA) and Tukey’s test at the significance level of P<0.05. Results: In ovarian histomorphometric studies, aspartame at a dose of 160 mg/kg significantly reduced growing follicles and significantly increased atresia follicles. Also in biochemical studies caused a significant decrease in TAC and a significant increase in MDA compared to control group. In connection with the studied genes, aspartame at a dose of 160 mg/kg caused a significant decrease in the expression of Bcl-2 gene and also a significant increase in the expression of P53 and Caspase-3 genes compared to the control group. Conclusion: It seems that high dose aspartame can cause adverse effects on histomorphology, histomorphometry and expression of P53, Bcl-2 and Caspase-3 genes in rat ovaries

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