Clostridium difficile toxin A is known to cause deacetylation of tubulin proteins, which blocks microtubule formation and triggers barrier dysfunction in the gut. Based on our previous finding that the Clostridium difficile toxin A-dependent activation of histone deacetylase 6 (HDAC-6) is responsible for tubulin deacetylation and subsequent microtubule disassembly, we herein examined the possible effect of potassium acetate (PA; whose acetyl group prevents the binding of tubulin to HDAC-6) as a competitive/false substrate. Our results revealed that PA inhibited toxin A-induced deacetylation of tubulin and recovered toxin A-induced microtubule disassembly. In addition, PA treatment significantly decreased the production of IL-6 (a marker of inflamed tissue) in the toxin A-induced mouse enteritis model. An in vitro HDAC assay revealed that PA directly inhibited HDAC-6-mediated tubulin deacetylation, indicating that PA acted as a false substrate for HDAC-6. These results collectively indicate that PA treatment inhibits HDAC-6, thereby reducing the cytotoxicity and inflammatory responses caused by C. difficile toxin A (1).
Sodium or potassium salts such as lactate and acetate can be used to inhibit the growth of spoilage bacteria and food-borne pathogens, and thereby prolong the shelf-life of refrigerated seafood. However, minimal information is available regarding the combined effects of potassium salts (acetate and lactate) with an agglomerated phosphate blend on the quality and safety of refrigerated catfish fillets. The objective of this study was to determine the microbiological and quality characteristics of marinated catfish fillets treated with organic acid salts. Catfish fillets were vacuum-tumbled with a brine solution with and without the added organic acid salts, at 10% over initial, raw weight prior to tray-packing and storage at 4 °C for 14 d. Fillets were evaluated for yields, color, pH, tenderness, consumer acceptability, and shelf-life. No differences (P > 0.05) existed among the treated and untreated fillets with regards to solution pick-up and pH, but all treated fillets increased (P < 0.05) cooking yields and Intl. Commission on Illumination (CIE) a* values, and decreased (P < 0.05) CIE L* and b* values in the catfish fillets when compared to the untreated fillets. The fillets treated with a combination of potassium acetate and potassium lactate had lower (P < 0.05) psychrotrophic plate counts and lower spoilage scores than the control treatments on days 7, 10, and 14. In addition, consumers preferred (P < 0.05) treated catfish fillets (fried) with respect to appearance, flavor, and overall acceptability over the negative control. In conclusion, the combination of potassium acetate and potassium lactate enhanced sensory quality and extended the shelf-life of refrigerated catfish fillets (2).
It is injected intravenously to patients in intensive care with potassium depletion (3).
References_______________________________________
(1) Potassium Acetate Blocks Clostridium difficile Toxin A-Induced Microtubule Disassembly by Directly Inhibiting Histone Deacetylase 6, Thereby Ameliorating Inflammatory Responses in the Gut.
Lu LF, Kim DH, Lee IH, Hong J, Zhang P, Yoon IN, Hwang JS, Kim H.
J Microbiol Biotechnol. 2016 Apr
(2) Potassium acetate and potassium lactate enhance the microbiological and physical properties of marinated catfish fillets.
Kin S, Schilling MW, Smith BS, Silva JL, Kim T, Pham AJ, Campano SG.
J Food Sci. 2011 May
(3) Preventing hypokalemia in critically ill patients.
Scotto CJ, Fridline M, Menhart CJ, Klions HA.
Am J Crit Care. 2014 Mar
Potassium acetate 
