Background: Zinc (Zn) level in prostatic tissue plays an important role in prostatic carcinogenesis and its measurement may be useful as a prostate cancer (PCa) biomarker.
Method: The present study evaluated by systematic analysis the published data for Zn content analyzed in cancerous prostates as well as in lateral and dorsal zones of normal glands. This evaluation reviewed 1885 studies, all of which were published in the years from 1921 to 2020 and were located by searching the databases PubMed, Scopus, ELSEVIER-EMBASE, Cochrane Library, and the Web of Science. The articles were analyzed and “Median of Means” and “Range of Means” were used to examine heterogeneity of the measured Zn content in prostates of men with PCa (PCa group) and in prostates of apparently healthy adult subjects (control group). The objective analysis was performed on data from the 57 studies, with 1295 subjects for the PCa group and from the 40 studies, with 1921 subjects for the control group.
Results: It was found that the range of means of prostatic Zn content reported in the literature varies widely: for cancerous gland from 3.3 mg/kg to 180 mg/kg with median of means 42 mg/kg and for peripheral zone of normal prostates from 27 mg/kg to 266 mg/kg with median of means 186 mg/kg on a wet mass basis. Ratios of means of Zn content in cancerous prostate (ZnPCa) to Zn content in normal gland (ZnN), both obtained by the same authors and methods, were also calculated.
Conclusion: Because of the uncertainties we have outlined, we recommend other primary studies should be performed.

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In many tissues, trace metals such as zinc (Zn), iron (Fe), and copper (Cu) are important for various physiological functions. However, it has been shown in humans and experimental animal models that excessive amounts of these trace metals in the body can induce various diseases in the central nervous system, liver, and respiratory tract. Although the role of zinc in the central nervous system is controversial, with some reports suggesting a protective role, we are interested in the negative effects of excessive amounts of zinc on the central nervous system. Previous studies suggest that zinc, which is released in excessive amounts after ischemic injury, is a major modulator of neuronal death, and that Zn²⁺-induced neuronal death is an important cause of dementia after ischemic injury. In addition, other trace metals are known to be present in the brain and/or cerebrospinal fluid. Thus, we have been analyzing the mechanisms by which zinc and other metals induce neuronal cell death. Recently, using immortalized hypothalamic neuronal cells (GT1-7 cells), we found that non-toxic concentrations of Cu²⁺ exacerbate Zn²⁺-induced neurotoxicity. Therefore, we will focus on the results of that research in this review.

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Metallothionein (MT) is a metalloprotein that has high affinity for heavy metal ions such as cadmium (Cd), copper, and mercury. We investigated the induction of MT expression by zinc (Zn) treatment of the cartilage precursor ATDC5 cell line using quantitative reverse transcription-polymerase chain reaction analysis. Cell viability and toxicity were examined by a WST-8 assay and lactate dehydrogenase assay, respectively. Zn treatment induced the expression of MT, which involved the differentiation of the ATDC5 cell line into chondrocytes. Treatment of ATDC5 cells with Cd caused a significant reduction in cell viability. However, following Zn pretreatment, there was no decrease in cell viability or differentiation on Cd treatment. Our study indicates that the induction of MT expression by Zn in cartilage precursor cells reduced Cd-associated cell toxicity.

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