Background and Objective Chronic kidney disease (CKD) is an important public health concern. With the decline of renal function, CKD patients gradually progress to end-stage kidney disease and need to undergo dialysis or kidney transplantation to maintain life, bringing a heavy economic burden to the family and society. Therefore, it is necessary to effectively prevent and delay the progression of CKD. Essential trace elements play an indispensable role in CKD, and the objective of this study is to systematically review their benefits in the disease and summarize the risks of their excess. Methods The keywords “trace elements”, “chronic kidney disease”, “dialysis”, “inflammation”, and “fibrosis” and their combinations were used to search for relevant literature published in the PubMed database and Web of Science. We then summarized the role of trace element abnormalities in CKD patients in anemia, oxidative stress, inflammation, and chronic fibrosis, and the risk of their excess. Key Content and Findings Imbalance of essential trace elements is a common complication of CKD and a risk factor for CKD progression, cardiovascular events, and death. This article reviews the effects of essential trace elements (iron, zinc, selenium, copper, iodine, and manganese) on CKD. We analyze literature and discuss the advantages and disadvantages of various essential trace elements. Conclusions Research shows CKD patients have an imbalance of essential trace elements, and treatment based on these is an important direction for future exploration. A knowledge of the homeostasis of trace elements is important to improving the prognosis of CKD patients and delaying the progression of the disease.

https://atm.amegroups.com/article/viewFile/107335/pdf

Benefits and risks of essential trace elements in chronic kidney disease: a narrative review

Testosterone and the Androgen Receptor.

Manganese (Mn) is an essential trace element, but insufficient or excessive bodily amounts can induce neurotoxicity. Mn can directly increase neuronal insulin and activate insulin-like growth factor (IGF) receptors. As an important cofactor, Mn regulates signaling pathways involved in various enzymes. The IGF signaling pathway plays a protective role in the neurotoxicity of Mn, reducing apoptosis in neurons and motor deficits by regulating its downstream protein kinase B (Akt), mitogen-activated protein kinase (MAPK), and mammalian target of rapamycin (mTOR). In recent years, some new mechanisms related to neuroinflammation have been shown to also play an important role in Mn-induced neurotoxicity. For example, DNA-sensing receptor cyclic GMP–AMP synthase (cCAS) and its downstream signal efficient interferon gene stimulator (STING), NOD-like receptor family pyrin domain containing 3(NLRP3)-pro-caspase1, cleaves to the active form capase1 (CASP1), nuclear factor κB (NF-κB), sirtuin (SIRT), and Janus kinase (JAK) and signal transducers and activators of the transcription (STAT) signaling pathway. Moreover, autophagy, as an important downstream protein degradation pathway, determines the fate of neurons and is regulated by these upstream signals. Interestingly, the role of autophagy in Mn-induced neurotoxicity is bidirectional. This review summarizes the molecular signaling pathways of Mn-induced neurotoxicity, providing insight for further understanding of the mechanisms of Mn.

Signaling Pathways Involved in Manganese-Induced Neurotoxicity

BACKGROUND
An increasing number of people have adhered to vegetarian diet since several years ago. Nowadays, the favorable effect of this dietary pattern on metabolic diseases is well established, but its impact on fertility and reproductive health as a serious health concern is not clear yet. Hence, we aim to summarize existing evidence, regarding the possible association between a vegetarian diet, and fertility as measured by key indicators such as sperm quality, and sex hormone levels.


METHODS
We systematically searched online databases, including PubMed, ISI, Scopus, and Google Scholar, up to December 1st, 2022 using relevant keywords. We included observational studies that compared semen quality, sex hormone levels, and infertility in people who adhered to a vegetarian diet versus. Heterogeneity between studies was assessed using I2 and Chi-square tests. Standardized mean differences (SMD) using a random/fixed model were calculated to assess outcomes between vegetarians and omnivores in included articles.


RESULTS
Finally, out of 972 documents that were retrieved, 20 articles met our inclusion criteria, and 16 were eligible for quantitative synthesis. Results of meta-analyses showed that there were no significant differences between vegetarians and omnivores in terms of semen quality parameters, including total sperm count, total and progressive sperm motility, sperm morphology, and sperm concentration. Seven studies on female sex hormones profiles were eligible for meta-analysis. The only significant difference was the lower level of plasma estrone in vegetarians (Pooled SMD: -0.56; 95% CI: -1.08, -0.05; P-value = 0.03) compared to the omnivores. Furthermore, our meta-analysis revealed significantly higher sex-hormone-binding globulin (SHBG) levels in vegetarians men than in omnivores (Pooled SMD: 0.52; 95% CI: 0.18, 0.86; P-value = 0.002).


CONCLUSION
Despite the numerous health benefits of a vegetarian diet, our review suggested that there were no conclusive positive or negative associations between vegetarian diet and semen quality, sex hormone levels, and infertility. Further studies are recommended to better understand vegetarian dietary pattern effect on infertility and reproductive health. This article is protected by copyright. All rights reserved.

The impact of vegetarian diet on sperm quality, sex hormones levels and fertility: A systematic review and meta-analysis.

Age, weight and circulating concentrations of total testosterone are associated with the relative prostatic size in adult intact male dogs.

Sex hormone-binding globulin, also known as testosterone-estradiol-binding globulin, is a multifunctional protein synthesised by hepatocytes. Sex hormone-binding globulin specifically binds and transports sex hormones to regulate plasma bioactive sex hormone levels and affects their bioavailability. As male sex hormone expression is dominated by testosterone, the binding of sex hormone-binding globulin with testosterone leads to the reduction in bioavailable testosterone, which cannot fulfil its physiological roles, thereby resulting in male infertility, erectile and gonadal dysfunction, prostate cancer and other male reproductive system diseases. Sex hormone-binding globulin may be involved in the pathogenesis of male reproductive system diseases, seriously affecting the quality of life of men. In this article, we review the association between sex hormone-binding globulin and male reproductive system diseases.

Research progress on the relationship between sex hormone-binding globulin and male reproductive system diseases

This study investigated hepatic oxidative damage in rats following long-term manganese (Mn) exposure and clarified the underlying mechanisms. Forty-eight rats (SPF, male) were randomly assigned to receive low (10 mg/kg, n = 16) or high doses of Mn (50 mg/kg, n = 16) or sterilized distilled water (control group, n = 16). Rats were euthanized after 12 months, and liver Mn levels and histopathological changes were determined. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and liver malondialdehyde (MDA), glutathione peroxidase (GSH-PX), nuclear factor E2-related factor-2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H quinine oxidoreductase-1 (NQO1) levels were also determined. The Mn concentration and relative liver weights were significantly higher in the high-dose Mn group than in the control and low-dose Mn exposure groups. Low-dose Mn exposure resulted in mild expansion of hepatic sinuses and intact nuclei, whereas high-dose exposure led to pathological alterations in hepatocytes. High-dose Mn treatment significantly increased AST, ALT, and MDA activities and decreased GSH-PX activity. Additionally, liver Nrf2, HO-1, and NQO1 protein expression were markedly reduced by Mn exposure. Under the study conditions, long-term low-dose Mn exposure resulted in slight pathological changes in liver structure, but high-dose Mn exposure affected both liver structure and function, which might be related to the inhibition of Nrf2 expression, suppression of the transcription of its underlying antioxidant genes, and down regulation of the corresponding proteins. Consequently, the antioxidant capacity in the rat liver was weakened.

Hepatic oxidative damage and Nrf2 pathway protein changes in rats following long-term manganese exposure.

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Research progress on the relationship between sex hormone-binding globulin and male reproductive system diseases

Hepatic oxidative damage and Nrf2 pathway protein changes in rats following long-term manganese exposure.