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<blockquote style="position: relative; padding-left: 55px;"><section><a href="https://pkteerium.xyz/objects/e14f7b96-b54e-44c1-89cc-f0c62f6b067e">cjd (cjd@pkteerium.xyz)'s status on Tuesday, 13-Dec-2022 08:56:31 JST</a><a href="https://pkteerium.xyz/users/cjd" title="cjd@pkteerium.xyz"><img src="https://gnusocial.jp/avatar/5316-48-20220814170603.webp" width="48" height="48" alt="cjd" style="position: absolute; left: 0; top: 0;">cjd</a><div><a href="https://mastodon.derveni.org/@arzachel/109503288011628846" rel="in-reply-to">in reply to</a><ul><li></ul></div></section><article>I was not able to find any evidence that Ivermectin has zinc ionophore effect (looking only at articles pre-2020 before everyone decided to just publish their political opinions as papers).<br><br>However I did find plenty of documentation about chloroquine acting as a zinc ionophore: e.g. <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109180">https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109180</a><br><br>And on the anti-viral effect of zinc: <a href="https://pubmed.ncbi.nlm.nih.gov/31305906/">https://pubmed.ncbi.nlm.nih.gov/31305906/</a><br><br>Ivermectin seems to be another beast entirely, but it is apparently effective as a cancer inhibitor: <a href="https://www.spandidos-publications.com/10.3892/mmr.2017.8231">https://www.spandidos-publications.com/10.3892/mmr.2017.8231</a> so definitely would not count it out.<br><br>But then again, science has not been reproducible for decades now, so are those papers really worth anything? ?♂️</article><footer><a rel="bookmark" href="https://gnusocial.jp/conversation/837133#notice-1608275">In conversation</a><time datetime="2022-12-13T08:56:31+09:00" title="Tuesday, 13-Dec-2022 08:56:31 JST">Tuesday, 13-Dec-2022 08:56:31 JST</time> <span>from <span><a href="https://pkteerium.xyz/objects/e14f7b96-b54e-44c1-89cc-f0c62f6b067e" rel="external" title="Sent from pkteerium.xyz via ActivityPub">pkteerium.xyz</a></span></span><a href="https://pkteerium.xyz/objects/e14f7b96-b54e-44c1-89cc-f0c62f6b067e">permalink</a><h4>Attachments</h4><ol><li><article><header><div>Domain not in remote thumbnail source whitelist: storage.googleapis.com</div><h5><a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109180">Chloroquine Is a Zinc Ionophore</a></h5><div></div></header><div>Chloroquine is an established antimalarial agent that has been recently tested in clinical trials for its anticancer activity. The favorable effect of chloroquine appears to be due to its ability to sensitize cancerous cells to chemotherapy, radiation therapy, and induce apoptosis. The present study investigated the interaction of zinc ions with chloroquine in a human ovarian cancer cell line (A2780). Chloroquine enhanced zinc uptake by A2780 cells in a concentration-dependent manner, as assayed using a fluorescent zinc probe. This enhancement was attenuated by TPEN, a high affinity metal-binding compound, indicating the specificity of the zinc uptake. Furthermore, addition of copper or iron ions had no effect on chloroquine-induced zinc uptake. Fluorescent microscopic examination of intracellular zinc distribution demonstrated that free zinc ions are more concentrated in the lysosomes after addition of chloroquine, which is consistent with previous reports showing that chloroquine inhibits lysosome function. The combination of chloroquine with zinc enhanced chloroquine's cytotoxicity and induced apoptosis in A2780 cells. Thus chloroquine is a zinc ionophore, a property that may contribute to chloroquine's anticancer activity.</div><footer></footer></article></li><li><article><header><div>Domain not in remote thumbnail source whitelist: cdn.ncbi.nlm.nih.gov</div><h5><a href="https://pubmed.ncbi.nlm.nih.gov/31305906/">The Role of Zinc in Antiviral Immunity - PubMed</a></h5><div></div></header><div>Zinc is an essential trace element that is crucial for growth, development, and the maintenance of immune function. Its influence reaches all organs and cell types, representing an integral component of approximately 10% of the human proteome, and encompassing hundreds of key enzymes and transcripti …</div><footer></footer></article></li><li><article><header><div>Domain not in remote thumbnail source whitelist: www.spandidos-publications.com</div><h5><a href="https://www.spandidos-publications.com/10.3892/mmr.2017.8231">Ivermectin as an inhibitor of cancer stem‑like cells</a></h5><div></div></header><div>The aim of the present study was to demonstrate that ivermectin preferentially inhibited cancer stem‑like cells (CSC) in breast cancer cells and downregulated the expression of ‘stemness’ genes. Computational searching of DrugBank, a database of approved drugs, was performed using the principles of two‑dimensional similarity searching; the chemical structure of salinomycin was used as a query. Growth inhibition of the breast cancer cell lin e MDA‑MB‑231 by ivermectin was investigated in the total cell population, in cell spheroids and in sorted cells that expressed cluster of differentiation (CD)44+/CD24‑. The effects of ivermectin treatment on the expression of pluripotency and self‑renewal transcription factors, such as homeobox protein nanog (nanog), octamer‑binding protein 4 (oct‑4) and SRY‑box 2 (sox‑2), were evaluated by reverse transcription‑quantitative polymerase chain reaction and western blotting. Ivermectin exhibited a similarity value of 0.78 in reference to salinomycin. Ivermectin demonstrated an inhibitory effect upon the growth of MDA‑MB‑231 cells in the range of 0.2‑8 µM. Ivermectin preferentially inhibits the viability of CSC‑enriched populations (CD44+/CD24‑ and cells growing in spheroids) compared with the total cell population. The opposite pattern was observed with paclitaxel treatment. Ivermectin exposure reduced the expression of nanog, oct‑4 and sox‑2 at the mRNA and protein levels. Ivermectin preferentially inhibited the CSC subpopulation in the MDA‑MB‑231 cells and downregulated the expression of genes involved in the maintenance of pluripotency and self‑renewal.</div><footer></footer></article></li></ol></footer></blockquote>

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cjd (cjd@pkteerium.xyz)'s status on Tuesday, 13-Dec-2022 08:56:31 JSTcjd
in reply to
- arzachel
I was not able to find any evidence that Ivermectin has zinc ionophore effect (looking only at articles pre-2020 before everyone decided to just publish their political opinions as papers).

However I did find plenty of documentation about chloroquine acting as a zinc ionophore: e.g. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109180

And on the anti-viral effect of zinc: https://pubmed.ncbi.nlm.nih.gov/31305906/

Ivermectin seems to be another beast entirely, but it is apparently effective as a cancer inhibitor: https://www.spandidos-publications.com/10.3892/mmr.2017.8231 so definitely would not count it out.

But then again, science has not been reproducible for decades now, so are those papers really worth anything? ?♂️
In conversationTuesday, 13-Dec-2022 08:56:31 JST from pkteerium.xyzpermalink
Attachments
1. Domain not in remote thumbnail source whitelist: storage.googleapis.com
  Chloroquine Is a Zinc Ionophore
  Chloroquine is an established antimalarial agent that has been recently tested in clinical trials for its anticancer activity. The favorable effect of chloroquine appears to be due to its ability to sensitize cancerous cells to chemotherapy, radiation therapy, and induce apoptosis. The present study investigated the interaction of zinc ions with chloroquine in a human ovarian cancer cell line (A2780). Chloroquine enhanced zinc uptake by A2780 cells in a concentration-dependent manner, as assayed using a fluorescent zinc probe. This enhancement was attenuated by TPEN, a high affinity metal-binding compound, indicating the specificity of the zinc uptake. Furthermore, addition of copper or iron ions had no effect on chloroquine-induced zinc uptake. Fluorescent microscopic examination of intracellular zinc distribution demonstrated that free zinc ions are more concentrated in the lysosomes after addition of chloroquine, which is consistent with previous reports showing that chloroquine inhibits lysosome function. The combination of chloroquine with zinc enhanced chloroquine's cytotoxicity and induced apoptosis in A2780 cells. Thus chloroquine is a zinc ionophore, a property that may contribute to chloroquine's anticancer activity.
2. Domain not in remote thumbnail source whitelist: cdn.ncbi.nlm.nih.gov
  The Role of Zinc in Antiviral Immunity - PubMed
  Zinc is an essential trace element that is crucial for growth, development, and the maintenance of immune function. Its influence reaches all organs and cell types, representing an integral component of approximately 10% of the human proteome, and encompassing hundreds of key enzymes and transcripti …
3. Domain not in remote thumbnail source whitelist: www.spandidos-publications.com
  Ivermectin as an inhibitor of cancer stem‑like cells
  The aim of the present study was to demonstrate that ivermectin preferentially inhibited cancer stem‑like cells (CSC) in breast cancer cells and downregulated the expression of ‘stemness’ genes. Computational searching of DrugBank, a database of approved drugs, was performed using the principles of two‑dimensional similarity searching; the chemical structure of salinomycin was used as a query. Growth inhibition of the breast cancer cell lin e MDA‑MB‑231 by ivermectin was investigated in the total cell population, in cell spheroids and in sorted cells that expressed cluster of differentiation (CD)44+/CD24‑. The effects of ivermectin treatment on the expression of pluripotency and self‑renewal transcription factors, such as homeobox protein nanog (nanog), octamer‑binding protein 4 (oct‑4) and SRY‑box 2 (sox‑2), were evaluated by reverse transcription‑quantitative polymerase chain reaction and western blotting. Ivermectin exhibited a similarity value of 0.78 in reference to salinomycin. Ivermectin demonstrated an inhibitory effect upon the growth of MDA‑MB‑231 cells in the range of 0.2‑8 µM. Ivermectin preferentially inhibits the viability of CSC‑enriched populations (CD44+/CD24‑ and cells growing in spheroids) compared with the total cell population. The opposite pattern was observed with paclitaxel treatment. Ivermectin exposure reduced the expression of nanog, oct‑4 and sox‑2 at the mRNA and protein levels. Ivermectin preferentially inhibited the CSC subpopulation in the MDA‑MB‑231 cells and downregulated the expression of genes involved in the maintenance of pluripotency and self‑renewal.

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