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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亜鉛（Zn）、銅（Cu）などの微量金属は、生体内に存在し、正常な生命機能を維持するために重要な役割を果たしている。一方、微量金属のホメオスタシスが崩壊すると、脳神経系、消化器系、呼吸器系などに異常をきたし、種々の疾患の発症原因となる。特に、脳神経系におけるZnの役割は注目されており、定常状態においてシナプス小胞内に蓄積しているZnが神経興奮時にシナプス間隙に放出された結果、神経細胞死が誘導され、アルツハイマー病などの神経疾患の発症に寄与することが報告されている。これまでに我々は Cu が Zn依存の神経細胞死を促進することを見出し、その神経細胞死の誘導機構や抑制因子を解析したので、本総説では我々の研究内容を概説する。

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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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