Sodium Copper Chlorophyllin (liquid chlorophyll) benefits

[cs3000]

Chlorophyllin is a derivative of chlorophyll, aka water soluble chlorophyll


Increases White blood count, Red blood count, Hemoglobin slightly, by 14 and 28 days , (from normal baselines, in rats with oxidative stress induced lowering of these i bet would be big effect)
https://www.cureus.com/articles/138...rent-injection-doses-of-liquid-chlorophyll#!/


There's about 4mg copper in 100mg chlorophyllin. (some supplement forms have magnesium instead of copper).

Think it's copper II which usually found as supplements that arent absorbed well. But iron chlorophyllin is as effective as heme iron for intestinal absorption , because the chlorophyllin helps intestinal transport (similar structure to hemoglobin).

I think the same thing happens with copper Analysis of the therapeutic effect of sodium copper chlorophyllin tablet in treating 60 cases of leukopenia - PubMed
low copper induces leukopenia , low neutrophils (but the neutrophils get deformed and pass through endothelial wall easier, which can play a role in many disorders)
sodium copper chlorophyllin fixes the leukopenia in humans
which makes me think the chlorophyllin is helping the copper absorb well


Helps heal colitis when given after colitis induction
https://www.researchgate.net/public...D_by_suppressing_autophagy_activation_in_mice

(i think dose = ~40mg human). visually looks like 50% healing

We further determined if the administration of CHL can relieve established colitis in mice. chlorophyllin was added to drinking water at 40 mg/L.
Strikingly, the DSS-induced mortality at 62.5% rate in mice at day 15 was substantially reduced by chlorophyllin treatment, showing a reduced mortality rate at 12.5%, which agreed with relieving symptoms of colitis

used topically way back for wound / ulcer healing

Its is a potent oxidative stress protector. scavenges free radicals directly, increases protective enzymes

maybe even more potent than glutathione for protecting mitochondria. protects DNA.
The Antioxidant and Free Radical Scavenging Activities of Chlorophylls and Pheophytins

https://pubmed.ncbi.nlm.nih.gov/11018464/

our results show that CHL is highly effective in protecting mitochondria, even at a low concentration of 10 microM. The antioxidant ability, at equimolar concentration, was more than that observed with ascorbic acid, glutathione, mannitol and tert-butanol. When CHL was fed to mice at a dose of 1% in drinking water, there was a significant reduction in the potential for oxidative damage in cell suspensions from liver, brain and testis.

https://www.jstage.jst.go.jp/article/cpb1958/32/2/32_2_716/_article

When sodium copper chlorophyllin (Cu-Chl-Na) was given intraperitoneally to rats (two doses of 50 or 100mg/kg at 18 and 2h prior to sacrifice), the soluble fraction of liver in injected animals showed an inhibition of the ascorbic acid- and NADPH-stimulated lipid peroxidation in hepatic microsomes from untreated rats.
These findings suggest that the administered Cu-Chl-Na or substance (s) derived from Cu-Chl-Na is taken into the liver and distributed among the mitochondria, microsomes and soluble fraction in an active form functioning as an antioxidant. Subsequently, a single injection of Cu-Chl-Na was observed to prevent effectively the impairment of hepatic microsomal functions (as indicated by the depression of glucose-6-phosphatase and drug-metabolizing enzyme system) resulting from ascorbic acid-induced lipid peroxidation.

Protects DNA in bone marrow at low dose <10mg orally
(but maybe needed higher dose to protect against the other compound?)

Fahey et al. [37] reported that chlorophyll can improve the function of essential detoxification pathways. Chlorophyllin was 410-fold more potent as a phase 2 enzyme inducer than chlorophyll, since it has other detoxification properties because it is much more water-soluble than chlorophyll. Antioxidant activity of chlorophyll from plant leave also reported by Sakagami et al. [38] showed that Sasa senanensis Rehder leaf extract containing Fe(II)-chlorophyllin demonstrated superoxide anion and hydroxyl radical-scavenging activity five times higher than a similar product containing Cu(II)-chlorophyllin and comparable to a product containing Cu(II)-chlorophyllin

https://www.eurekaselect.com/article/112815

Conclusion: Therefore, the present study reports, for the first time, the screening of phytobased bioactive CHL for preventing/limiting the extent of food-additive-induced genotoxicity and mitochondrial dysfunction and serves as an advanced therapeutic tool in the management of diabetes.

Dual actions of the antioxidant chlorophyllin, a glutathione transferase P1-1 inhibitor, in tumorigenesis and tumor progression - PubMed in vivo treatment with chlorophyllin increased the GSH levels in the liver and significantly decreased DNA damage in the blood, liver, and tumor tissues. Even though tumorigenesis was delayed in rats receiving chlorophyllin before MNU injections, once the tumors emerged, the progression of tumor appeared to be faster than in the animals that received the carcinogen only [what's good for healthy cells can also be good for cancer cells] Chlorophyllin displayed genoprotective effects that initially delayed tumorigenesis. However, once the tumors were established, it may act as a promoter that facilitates tumor growth, potentially by a mechanism independent of cell proliferation and viability. Our results underline the pros and cons of antioxidant treatment in cancer, even if it has a capacity to inhibit GST P1-1.

Chlorophyllin disables potent carcinogens such as polycyclic aromatic hydrocarbons and heterocyclic amines by forming complexes with these chemicals that limit the ability of these toxins to bind to normal cells to inflict malignant changes

It's similar in structure to hemoglobin so also binds iron (iron chlorophyllin is as effective as heme iron for intestinal absorption) , and might be another mechanism behind its anti-carcinogen properties by oxidizing them, so could have dual properties (i guess re-releases the iron as its shown to help raise red blood counts?)

DNA protective against radiation and other oxidative stressors
250mg lowest dose tested was just as effective as more which implies no further benefit from 250mg. (effect should work at lower amounts too)

nice effect on small intestine in liver fibrosis / cirrhosis
https://www.frontiersin.org/files/A...09-01671-HTML/image_m/fphys-09-01671-g004.jpg

In an animal model, dietary supplementation of chlorophyllin at 4 mg/kg body weight inhibited the development of MNNG-induced fore stomach carcinoma.

In this study we found that chlorophyllin is able to ameliorate the hepatic toxin induced liver fibrosis. Mechanistically, chlorophyllin may work on two levels. First, we found that chlorophyllin can directly impact intestinal epithelial cells and suppress inflammatory signals that are initiated by LPS and TNF-alpha.

In particular, administration of chlorophyllin can promptly restore eubiosis, showing restoration of Bacteroidetes and reduction of Firmicutes Such a finding is important because it can also explain the observed reduction of plasma endotoxin, preassembling through the prevention of the death of Bacteroidetes, the Gram-negative bacteria that may contribute to the plasma endotoxin via intestinal-hepatic circulation.

inhibits kidney stone growth / oxalates Effect of sodium copper chlorophyllin on the formation of calcium oxalate crystals in rat kidney - PubMed

 

[cs3000]

Chlorophyll-Mediated Changes in the Redox Status of Pancreatic Cancer Cells Are Associated with Its Anticancer Effects

Interesting one. Antioxidants often linked to more cancer metastasis / growth , because they protect healthy cells & also cancer cells from ROS.
But here chlorophyll A inhibited pancreatic tumor , grew 1/3 size compared to placebo.
while potently reducing mitochondrial ROS when fed to mice, on low dose

in our in vitro study on human pancreatic cancer cells, we demonstrated the potent antiproliferative activities for all tested chlorophylls and found that chlorophyll a was the most effective. chlorophyll a treatment was initiated by intragastric administration once daily via a gastric tube (1.5 mg/kg body weight/day) for 30 days.

** "Importantly, mitochondrial ROS govern the cellular redox signaling, and an increase in their production has been shown to be critical for tumorigenesis" <---- so antioxidants can protect cancer cells from outside ROS damage , but on the other hand those that lower mitochondrial ROS inside cancer cells can slow growth
In cancer cells, mitochondrial ROS amplify the tumorigenic phenotype and accelerate the accumulation of additional mutations that lead to metastatic behaviour. As mitochondria carry out important functions in normal cells, disabling their function is not a feasible therapy for cancer. However, ROS signalling contributes to proliferation and survival in many cancers, so the targeted disruption of mitochondria-to-cell redox communication represents a promising avenue for future therapy.

The enhanced generation of mitochondrial ROS in the hypoxic tumour microenvironment represents an important mechanism promoting growth, metabolic reprogramming and survival, as these oxidants can act both as signalling molecules and by damaging DNA. The mutant mtDNA-containing cells grew faster than wild-type cells in immunocompromised mice, suggesting that mutations in mtDNA have the potential to alter the phenotype in an existing tumour cell line. Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles’ heel?

several reports suggest that supplementation with antioxidants including N-acetylcysteine and tocopherol may, in fact, promote the progression of cancer through their protection against oxidative stress [44, 45]. However, here, we report that chlorophylls, in contrast to other antioxidants, suppressed the progression of pancreatic cancer. This effect was accompanied by attenuated expression and activity of HMOX1, a crucial component of the intrinsic cellular antioxidant system. [Chlorophyllin also decreased HMOX1 expression in the cancer cells in this study a similar amount, and activity even more. but chlorophyllin didnt lower the cell viability like chlorophyll A did].
This might really have relevance to their anticancer effects, since HMOX1 expression has been reported to prevent the responsiveness of pancreatic cancer to cytostatic therapy [17]. It is interesting to note that this effect might be (cancer) cell-specific, since the opposite activity against HMOX1 expression was observed for chlorophyllin-treated human umbilical vein endothelial cell
Interestingly, we did not observe any effect of chlorophylls on glutaminolysis or reductive carboxylation, indicating that neither glycolysis nor mitochondrial respiration was affected by chlorophyll treatment [25]. Hence, it seems that the antiproliferative effects of chlorophylls are related to the suppression of ROS production and are unrelated to cell bioenergetics. In previous studies, chlorophyllin was reported to downregulate the PI3K/Akt signaling pathway [29] and shown to inhibit the proliferation of MCF-7 breast carcinoma cells by deactivating ERK [28]. However, neither chlorophyll a nor chlorophyllin had any inhibitory effect on AKT or ERK phosphorylation in our pancreatic cancer cell studies.

in another study opposite effects are shown on colon cancer by Chlorophyllin, increasing growth instead. Chlorophyllin, an antimutagen, acts as a tumor promoter in the rat-dimethylhydrazine colon carcinogenesis model - PubMed

So either:
1. this beneficial effect may be specific to certain cancers like pancreatic cancer , and opposite on others
or 2. it might be more of a dose sensitive effect (dosing things too high show opposite effects often) i think high dose was used in the colon study? they put 1 gram in the drinking water, but don't say for what amount of water, guess per liter?. small doses used in the pancreatic cancer study
Promotion versus suppression of rat colon carcinogenesis by chlorophyllin and chlorophyll: modulation of apoptosis, cell proliferation, and β-catenin/Tcf signaling

Promotion versus suppression of rat colon carcinogenesis by chlorophyllin and chlorophyll: modulation of apoptosis, cell proliferation, and β-catenin/Tcf signaling

Promotion versus suppression of rat colon carcinogenesis by chlorophyllin and chlorophyll: modulation of apoptosis, cell proliferation, and β-catenin/Tcf signaling

www.academia.edu

We therefore sought to compare the activities of chlorophyllin and chlorophyll using a post-initiation ACF protocol in the rat (Fig. 4b). Rats were initiated with IQ or azoxymethane (AOM), a metabolite of DMH, and because of the low water solubility of chlorophyll, dietary rather than drinking water exposures were chosen for the test agents. Post-initiation exposures were as follows: 0.24% chlorophyllin in the diet (approximates the daily intake from 0.1% chlorophyllin in the drinking water); 0.08% chlorophyll in the diet (approximates the daily chlorin intake from 0.24% chlorophyllin [11]); 0.0032% Cu(assumes the complete release of copper from 0.24% chlorophyllin); and 0.03% phytol (assumes the cleavage of all phytol groups from 0.08% chlorophyll).
In this experiment, chlorophyll suppressed the development of AOM- and IQ-induced ACF modestly but significantly, although this was largely restricted to the smaller foci containing one to three aberrant crypts per ACF (Fig. 4c and d). In the other treatment groups, changes in the number or size of foci were not statistically significant, except for a slight increase in the smallest foci following treatment with IQ plus Cu. 0.001% chlorophyllin caused an apparent increase in the rate of cell proliferation versus apoptosis, whereas higher chlorophyllin concentrations failed to increase, and indeed modestly reduced this ratio in the colonic crypt. the lowest concentration of 0.001% chlorophyllin promoted and intermediate concentrations of 0.01 and 0.1% chlorophyllin had no effect, but 1.0% chlorophyllin suppressed IQ-induced ACF significantly

^ by this Chlorophyl has better anti cancer properties and Chlorophyllin can have opposite , at least shown in colon, depending on dose


Dietary chlorophyllin inhibits the canonical NF-κB signaling pathway and induces intrinsic apoptosis in a hamster model of oral oncogenesis - PubMed but here 4mg/kg Chlorophyllin in hamsters actually induced apoptosis in defective cells from carcinogens & prevented mouth carcinomas. which is ~35mg human dose. its complicated

or 3. chlorophyl A has better cancer specific effects and chlorophyllin can have opposite in vivo , at least in the colon Natural Chlorophyll but Not Chlorophyllin Prevents Heme-Induced Cytotoxic and Hyperproliferative Effects in Rat Colon

In fact, in all of the tested chlorophylls, concentrations as low as 10 μM substantially decreased mitochondrial superoxide production in pancreatic cancer cells (Figure 4). Additionally, when exposed to any of the tested chlorophylls, increased proportions of reduced glutathione were observed in the pancreatic cancer cells, suggesting an attenuated production of intracellular oxidants (Figure 5). Furthermore, hydrogen peroxide production by human pancreatic cancer cells was also significantly affected by higher concentrations of the tested chlorophylls (50 μmol/L (Figure 6)) while lower concentrations showed no effect (10 μmol/L, data not shown).

<- (it shrank on day 29?)

maybe best bet could be to take a mix of Chlorophyl A and Chlorophyllin for balance

 

[youngsinatra]

Interesting

 

[cs3000]

Gonna try it , probably a mix of both forms
*not sure if it works the same in humans but better to avoid if pregnant just incase
https://pubmed.ncbi.nlm.nih.gov/12395407/
https://www.medigraphic.com/cgi-bin/new/resumenI.cgi?IDARTICULO=11967
as in mice in these studies it induced loss of their litter (higher mitochondrial ROS needed during development or something? not sure of mechanism)

but in this study it was opposite, litter size went up and 13 were born vs 9 Identifying efficacious approaches to chemoprevention with chlorophyllin, purified chlorophylls and freeze-dried spinach in a mouse model of transplacental carcinogenesis
"We observed no overt adverse effects of any treatment regimen on dams or offspring (e.g. no difference in birth weight, litter size, etc."
so idk the differences. possible higher dose in the last study had reverse effect (which might not function properly for the other desired effects).
but something to know