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  3. Acetic acid lead

Acetic acid lead is a carboxylic acid and short-chain fatty acid (SCFAs). Magnesium acetate tetrahydrate activates AMPK, increases ROS, cleaved caspase 9, PPARα, downregulates SREBP-1c, ChREBP expression. Acetic acid lead exhibits antifungal activity against Saccharomyces cerevisiae W303-1A. Acetic acid lead regulates energy metabolism. Acetic acid lead has anticancer activity against gastric cancer. Acetic acid lead induces writhing reaction and ulcerative colitis. Acetic acid lead can be used in the researches for gastric cancer, ulcerative colitis, hepatic steatosis, and pain.

For research use only. We do not sell to patients.

Acetic acid lead

Acetic acid lead Chemical Structure

CAS No. : 546-67-8

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Description

Acetic acid lead is a carboxylic acid and short-chain fatty acid (SCFAs). Magnesium acetate tetrahydrate activates AMPK, increases ROS, cleaved caspase 9, PPARα, downregulates SREBP-1c, ChREBP expression. Acetic acid lead exhibits antifungal activity against Saccharomyces cerevisiae W303-1A. Acetic acid lead regulates energy metabolism. Acetic acid lead has anticancer activity against gastric cancer. Acetic acid lead induces writhing reaction and ulcerative colitis. Acetic acid lead can be used in the researches for gastric cancer, ulcerative colitis, hepatic steatosis, and pain[1][2][3][4][5][6][7][8][9].

In Vitro

Acetic acid lead (Acetic acid; 2-5 µM; 24 h) induces cancer cell-selective death in gastric cancer cells (RGK1) via oxidative stress, while having minor effects on normal gastric mucosal cells (RGM1)[3].
Acetic acid lead (Acetic acid; 20-200 mM; 200 min) induces programmed cell death in Saccharomyces cerevisiae W303-1A[4].
Acetic acid lead (Acetic acid; 5 mM; 15 d) suppresses the increase in disaccharidase activity (sucrase, maltase, trehalase, lactase) in Caco-2 cells without affecting cell growth or glucose transport[5].
Acetic acid lead (Acetic acid; 8-7.2 mM; 3 h) activates the AMPKα signaling pathway by consuming ATP to increase the AMP/ATP ratio in bovine hepatocytes, upregulating lipid oxidation genes, downregulating lipogenic genes, and reducing intracellular triglyceride content[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[3]

Cell Line: Rat gastric mucosal cells (RGM1), cancerous gastric mucosal cells (RGK1)
Concentration: 0, 1, 2, 5, 10, 20 µM
Incubation Time: 24 h
Result: Increased monocarboxylic transporter 1 (MCT1) and cleaved caspase 9 in RGK1 cells.
Showed minor effects in RGM1 cells.
In Vivo

Acetic acid lead (0.10-0.56%; i.p.; single dose) produces concentration-dependent suppression of feeding behavior and robust writhing in male C57BL/6J mice, with maximal effects from the 0.56% dose lasting up to 60 minutes for feeding suppression[7].
Acetic acid lead (5% v/v; i.r.; single dose) induces severe ulcerative colitis in male Kunming mice, characterized by high mortality, increased disease activity index, colon tissue damage, elevated neutrophil infiltration, and upregulated pro-inflammatory cytokine and NF-κB p65 expression[8].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: C57BL/6J (male, 20-33g)[7]
Dosage: 0.10%; 0.18%; 0.32%; 0.56%
Administration: i.p.; single dose
Result: Reduced Ensure consumption to 0.09 g/g body weight at 0.32% dose, significantly lower than control 0.14 g/g body weight.
Reduced Ensure consumption to 0.03 g/g body weight at 0.56% dose, significantly lower than control 0.14 g/g body weight.
Induced a mean of approximately 32 writhes over 20 minutes at 0.56% dose.
Produced significant feeding-suppressant effects at 0 and 60 minutes post-administration with 0.56% dose, which were no longer apparent by 240 minutes post-administration.
Animal Model: Kunming mice (male, 20-25 g)[8]
Dosage: 5% v/v
Administration: i.r.; single dose
Result: Caused severe colitis with bloody diarrhea, poor coat quality, dramatic body weight loss, reduced mobility, and gross blood adhesion to the anus.
Resulted in a high mortality rate.
Led to 78.44% colon area affected.
Caused wet colon weight/length of 162.8 mg/cm.
Resulted in a macroscopic score of ~3.8.
Induced a histological score of ~3.9.
Increased colonic MPO activity to ~2.4 U/g tissue.
Elevated serum and colonic TNF-α and IL-6.
Distinctly elevated p65 NF-κB protein expression compared to normal controls.
Molecular Weight

447.43

Formula

C2H4O2.1/4Pb

CAS No.
SMILES

CC([O-])=O.[0.25Pb4+]

Structure Classification
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Acetic acid lead
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HY-Y0319D
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