Studies have reported the adverse effects of hyperuricemia on male reproduction, but the mechanism is still unclear. The purpose of this study is to explore the mechanism of hyperuricemia on reproductive system damage in male rats. The rats were divided into a control group and a model group. Rats were given hypoxanthine and potassium oxonate dissolved in 0.5% (w/v) sodium carboxymethyl cellulose solution to induce the hyperuricemia (HUA) model. After 6 weeks, the blood, testis, and epididymis tissues of the anesthetized rats were collected for further experiments and analysis. Compared with the control rats, the serum uric acid of HUA rats was significantly increased, and the serum testosterone, sperm count, and motility were significantly decreased. The protein expression of testosterone-related molecules CYP11A1, 3β-HSD, and StAR was downregulated in the testis of HUA rats. The protein expression of blood–testis barrier (BTB) related molecules ZO-1 and Connexin43 was downregulated in the testis of HUA rats. Compared with the control group, the zinc content and zinc-containing enzymes (ALP and LDH) were decreased, and the mRNA and protein expression of zinc transporters (ZnT4 and ZIP7) were downregulated in the testis of HUA rats. Furthermore, the level of MDA increased and the activities of CAT, GSH-PX, and SOD decreased in the testicular tissue of HUA rats. The PI3K/AKT/mTOR pathway in the testis of HUA rats was activated. However, there was no significant change in the protein expression of autophagy associated molecules LC3, Beclin1, and ATG5 in the testis of HUA rats. Thus, the conclusion is that hyperuricemia can lead to the destruction of BTB, impaired testosterone synthesis, and decreased sperm count and motility in male rats, mainly by inducing zinc homeostasis imbalance and oxidative stress, rather than autophagy.

Objective To determine the possible protective effects of Jinghuosu, a dietary supplement (DS), on tripterygium glycosides (TG)-induced reproductive system injury in rats and its underlying mechanisms. Methods A reproductive damage model was established in rats by feeding of TGs. Twenty-eight male Sprague Dawley rats were randomly divided into 4 groups using a random number table ( n =7 in each): control (C) group, model (M) group, DS group and L-carnitine (LC) group. Rats in M, DS and LC groups received 40 mg/kg TGs orally. Starting from the 5th week, after administration of TGs for 4 h every day, rats in DS and LC groups were administered with 2.7 g/kg DS and 0.21 g/kg LC, respectively, for protective treatment over the next 4 weeks. Rats in Group C continued to receive the control treatment. Hematoxylin-eosin staining was used for histopathological analysis of rat testicular tissues. Enzyme-linked immunosorbent assay was performed to measure alkaline phosphatase (ALP), lactate dehydrogenase, alcohol dehydrogenase, total antioxidant capacity (T-AOC), superoxide dismutase, glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) concentrations. Chemiluminescence assay was used to determine the serum testosterone content. Quantitative real-time PCR and Western blotting were conducted to analyze the expression of genes and proteins related to the testosterone synthesis pathway and the nuclear factor erythroid 2-related factor 2/heme oxygenase 1 antioxidant pathway. Results Oral administration of TGs induced significant increases in the testicular levels of zinc transporter 1 and MDA ( P <0.05). On the other hand, sperm concentration, sperm motility, and serum testosterone, serum zinc, testicular zinc, Zrt-, Irt-like protein 1, ALP, luteinizing hormone (LH) receptor, steroidogenic acute regulatory protein, Cytochrome P450 family 11 subfamily A member 1, 3 β -hydroxysteroid dehydrogenase 1 T-AOC, GSH-Px, nuclear factor erythroid 2-related factor 2, heme oxygenase-1 and NAD (P)H: quinone oxidoreductase 1 levels decreased following TGs exposure ( P <0.05). All of these phenotypes were evidently reversed by DS ( P <0.05). Conclusion DS Jinghuosu protects against TG-induced reproductive system injury in rats, probably by improving zinc homeostasis, enhancing the testosterone synthesis and attenuating oxidative stress.

Background: Zinc (Zn)is an essential trace element for spermatogenesis and its deficiency causes abnormal spermatogenesis. Objective: The present study was conducted to examine the mechanisms by which Zn-deficient diet impairs sperm morphology and its reversibility. Methods: 30 SPF grade male Kunming (KM) mice were randomly divided into three groups, 10 mice per group. Zn-normal diet group (ZN group) was given Zn-normal diet(Zn content= 30 mg/kg)for 8 weeks. Zn-deficienct diet group (ZD group) was given Zn-deficienct diet(Zn content< 1 mg/kg)for 8 weeks. Zn-deficient and Znnormal diet group(ZDN group)was given 4 weeks Zn-deficienct diet followed by 4 weeks Zn-normal diet. After 8 weeks, the overnight fasted mice were sacrificed, and blood and organs were collected for further analysis. Results: The experimental results showed that Zn-deficienct diet leads to increased abnormal morphology sperm and testicular oxidative stress.The rate of abnormal morphology sperm, chromomycin A3(CMA3), DNA fragmentation index (DFI), malondialdehyde (MDA) were significantly increased, and a-kinase anchor protein 4 (AKAP4), dynein axonemal heavy chain 1(DNAH1), sperm associated antigen 6(SPAG6), cilia and flagella associated protein 44(CFAP44), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), total antioxidant capacity (T-AOC), nuclear factor erythroid 2-related factor (NRF2), NAD(P)H:quinone oxidoreductase 1(NQO1) and heme oxygenase 1(HO1) were significantly decreased in the ZD group mice. While the changes in above indicators caused by Zn-deficient diet were significantly alleviated in the ZDN group. Conclusion: It was concluded that Zn-deficient diet causes abnormal morphology sperm and testicular oxidative stress in male mice. Abnormal morphology sperm caused by Zn-deficient diet are reversible, and Zn-normal diet can alleviate them.

Zinc is a vital trace element for normal function of the living system. In male, zinc is involved in various biological processes, an important function of which is as a balancer of hormones such as testosterone. For this purpose, studies related to the influence of zinc on serum testosterone were selected and summarized, including the effect of dietary zinc deficiency and zinc supplementation on testosterone concentrations. After preliminary searching of papers on databases, 38 papers including 8 clinical and 30 animal studies were included in this review. We concluded that zinc deficiency reduces testosterone levels and zinc supplementation improves testosterone levels. Furthermore, the effect degree of zinc on serum testosterone may vary depending on basal zinc and testosterone levels, zinc dosage form, elementary zinc dose, and duration. In conclusion, serum zinc was positively correlated with total testosterone, and moderate supplementation plays an important role in improving androgen.

As a marker of inflammation, calprotectin has potential application value in a variety of inflammatory diseases, such as arthritis and bacterial infections. Clostridioides difficile infection (CDI) is an infectious disease that causes intestinal damage and inflammation. This systematic review aims to determine whether fecal calprotectin has application value in CDI. Nine databases were searched from inception to 6 June 2022, and 17 studies were included. These studies were divided into four groups according to their content. Generally speaking, fecal calprotectin is not an ideal indicator for the diagnosis and prognosis prediction of CDI but may serve as a potential indicator for assessing disease severity and as a readily detectable marker for CDI screening. In addition, patients in need of treatment or with detectable toxins in stool may tend to have higher levels of fecal calprotectin. In summary, fecal calprotectin has some potential application value in CDI. However, further studies are needed to verify these findings and determine the reliability of calprotectin as a biomarker for CDI.

Zinc (Zn) is an essential trace element for human growth and its deficiency causes huge health impacts. The present study was conducted to examine the mechanisms by which Zn-deficient diet impairs reproductive function and its reversibility. Hence, SPF grade male Kunming (KM) mice were divided into three groups. Zn-normal diet group (ZN group) was provided with Zn-normal diet (Zn content = 30 mg/kg, DY19410Y) for 8 weeks. Zn-deficient diet group (ZD group) was provided with Zn-deficient diet (Zn content < 1 mg/kg, DY19401) for 8 weeks. Zn-deficient and Zn-normal diet group (ZDN group) was provided with 4 weeks Zn-deficient diet followed by 4 weeks Zn-normal diet. After 8 weeks, the overnight-fasted mice were sacrificed, and blood and organs were collected for further analysis. The results showed that Zn-deficient diet caused testicular structural disorders, decreased semen quality, imbalance in zinc homeostasis, and impaired autophagy. Semen quality, testosterone, serum Zn, testicular tissue Zn, testicular free Zn ions, alkaline phosphatase (ALP), zinc transporter 7(ZnT7), Beclin1, autophagy-related 5(ATG5), and the ratio of light chain 3(LC3) II/LC3I were significantly decreased, and ZnT4, Zrt-, Irt-like protein7 (ZIP7), and ZIP13 expression were significantly increased in ZD group mice, while the changes in above indicators caused by Zn-deficient diet were significantly alleviated in the ZDN group. It was concluded that Zn-deficient diet causes testicular structural disorders and decreased semen quality by causing imbalances in Zn homeostasis and impaired autophagy in male mice. Reproductive damages caused by Zn-deficient diet are reversible, and Zn-normal diet can alleviate them.