Cyanide and lactate levels in patients during chronic oral amygdalin intake followed by intravenous amygdalin administration

Mani, Jens; Rutz, Jochen; Maxeiner, Sebastian; Juengel, Eva; Bon, Dimitra; Roos, Frederik C.; Chun, Felix K.‐H.; Blaheta, Roman A.

doi:10.1016/j.ctim.2019.03.002

Cited by 20 publications

(6 citation statements)

References 22 publications

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“…In addition, there was a significant increase in the LPO level in the hepatic (33.160 ± 1.337 nmol/g; P < 0.05) and testicular tissues (13.043 ± 0.134 nmol/g; P < 0.05) compared with that in the control group. The toxicity and efficacy of amygdalin in animal models have not been fully investigated, however it has been reported that orally administered amygdalin releases a high amount of cyanide (Mani et al, 2019). Amygdalin can be converted into hydrocyanic acid via the action of emulsion complex enzymes (Zhou et al, 2012) that contain β-D-glucosidase, which is found in foods, and microflora of the colon and small intestine (Blaheta et al, 2016); amygdalin can also undergo hydrolysis without enzymatic catalysis (Holzbecher, Moss & Ellenberger, 1984;Strugala et al, 1995), also it can be hydrolyzed by water into glucose, benzaldehyde, and hydrocyanic acid; however, boiling water causes amygdalin to epimerize (Savic et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the effective dose of amygdalin for the improvement of antioxidant gene expression and suppression of oxidative damage in mice

Albogami

Hassan

Ahmed

et al. 2020

PeerJ

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Background Little is known regarding the toxic and therapeutic doses of amygdalin. Treatment regimens and schedules can vary between humans and animal models, and there have been reports of cyanide toxicity due to amygdalin use. Objective The aim of this study was to evaluate the effect of different doses of amygdalin on antioxidant gene expression and suppression of oxidative damage in mice. Methods Forty adult male mice were divided randomly into four groups (n = 10) as follows and treated orally for two weeks: a control group treated with saline solution, a group treated with amygdalin at 200 mg/kg body weight, a group treated with amygdalin at 100 mg/kg body weight, and a group treated with amygdalin at 50 mg/kg body weight. Liver and testis samples were collected for gene expression, biochemical and histopathological analyses. Results The mice treated with medium-dose amygdalin (100 mg/kg) showed upregulated mRNA expression of glutathione peroxidase (P < 0.01) and superoxide dismutase (P < 0.05) and significantly decreased lipid peroxidation (P < 0.05) in hepatic and testicular tissues compared to those in the untreated groups (controls), with mild histopathological effects. The mice treated with high-dose of amygdalin (200 mg/kg) showed downregulated mRNA expression of glutathione peroxidase and superoxide dismutase (P < 0.01) and significantly increased lipid peroxidation (P < 0.05) in both hepatic and testicular tissues compared to those in the untreated groups (controls), with an apparent effect at the histopathological level. No effects were observed in the mice treated with low-dose amygdalin (50 mg/kg) at the gene, protein and histopathological level. Conclusion Low-and medium-dose amygdalin did not induce toxicity in the hepatic and testicular tissues of male mice, unlike high-dose amygdalin, which had a negative effect on oxidative balance in mice. Therefore, amygdalin at a moderate dose may improve oxidative balance in mice.

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Section: Discussionmentioning

confidence: 99%

Evaluation of the effective dose of amygdalin for the improvement of antioxidant gene expression and suppression of oxidative damage in mice

Albogami

Hassan

Ahmed

et al. 2020

PeerJ

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“…The amygdalin concentration in the blood was very high after the intravenous injection, and very little cyanide was available [ 136 ], and a precursor to amygdalin could be seen in the plasma. Although amygdalin was primarily eliminated in its unique form via urine following venous infusion, the peak defecation rate occurred 2 h after infusion, and the cumulative flow degree by 24 h was 79.6% [ 137 ]. Research suggests that amygdalin administered intravenously avoids breakdown by digestive enzymes and produces no cyanide toxicity in combination with its ineffectiveness.…”

Section: Toxicological Effects Of Amygdalinmentioning

confidence: 99%

Amygdalin: A Review on Its Characteristics, Antioxidant Potential, Gastrointestinal Microbiota Intervention, Anticancer Therapeutic and Mechanisms, Toxicity, and Encapsulation

et al. 2022

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Bioactive amygdalin, found in high concentrations in bitter almonds, has been recognized as a symbol of the cyanogenic glycoside chemical organic substance, which was initially developed as a pharmaceutical for treating cancer after being hydrolyzed to hydrogen cyanide (HCN). Regrettably, research has shown that HCN can also damage normal cells, rendering it non-toxic to the human body. Extreme controversy surrounds both in vivo and in vitro studies, making its use risky. This review provides an extensive update on characteristics, antioxidant potential, gastrointestinal microbiota intervention, anticancer therapeutic, mechanisms, toxicity, and encapsulation of amygdalin. Antioxidant, anti-tumor, anti-fibrotic, antiatherosclerosis, anti-inflammatory, immunomodulatory, and analgesic characteristics, and the ability to improve digestive and reproductive systems, neurodegeneration, and cardiac hypertrophy are just some of the benefits of amygdalin. Studies verified the HCN-produced amygdalin to be harmful orally, but only at very high doses. Although intravenous treatment was less effective than the oral method, the oral route has a dose range of 0.6 to 1 g daily. Amygdalin’s toxicity depends heavily on the variety of bacteria in the digestive tract. Unfortunately, there is currently no foolproof method for determining the microbial consortium and providing a safe oral dosage for every patient. Amygdalin encapsulation in alginate-chitosan nanoparticles (ACNPs) is a relatively new area of research. Amygdalin has an enhanced cytotoxic effect on malignant cells, and ACNPs can be employed as an active drug-delivery system to release this compound in a regulated, sustained manner without causing any harm to healthy cells or tissues. In conclusion, a large area of research for a substance that might be the next step in cancer therapy is opened up due to unverified and conflicting data.

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“…Although cyanide synthesis by mammalian cells has not been investigated extensively, several studies indicate that mammals have detectable circulating cyanide concentrations, and cyanide production has been demonstrated in various mammalian cells and tissues. Utilizing a variety of methods the basal circulating cyanide concentration in healthy volunteers has been estimated to be in the range of 1–5 µ m [ 173 , 174 , 175 , 176 , 177 ]. Perhaps these methods overestimate the concentration of cyanide, at least in part because some of these methods may also include thiocyanide.…”

Section: Endogenous Generation Of Cyanide In Mammalian Cellsmentioning

confidence: 99%

The two faces of cyanide: an environmental toxin and a potential novel mammalian gasotransmitter

Zuhra

Szabó

2021

The FEBS Journal

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Cyanide and lactate levels in patients during chronic oral amygdalin intake followed by intravenous amygdalin administration

Cited by 20 publications

References 22 publications

Evaluation of the effective dose of amygdalin for the improvement of antioxidant gene expression and suppression of oxidative damage in mice

Evaluation of the effective dose of amygdalin for the improvement of antioxidant gene expression and suppression of oxidative damage in mice

Amygdalin: A Review on Its Characteristics, Antioxidant Potential, Gastrointestinal Microbiota Intervention, Anticancer Therapeutic and Mechanisms, Toxicity, and Encapsulation

The two faces of cyanide: an environmental toxin and a potential novel mammalian gasotransmitter

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