Studies on the Anticandidal Mode of Action of Allium sativum (Garlic)

Mahmoud A. Ghannoum

Microbiology · 1988 · 135 citations · 26 references

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TL;DR

The study investigated the mode of action of aqueous garlic extract (AGE) against Candida albicans. AGE acts by oxidizing thiol groups in essential proteins, leading to enzyme inactivation and growth inhibition, as shown by growth antagonism, enzymic inhibition, and zone interference studies. AGE inhibited six clinical Candida albicans isolates with MICs of 0.8–1.6 mg ml⁻¹, disrupted cell surface integrity and lipid composition, reduced oxygen consumption, and its activity was antagonized by thiols such as L‑cysteine, glutathione, and 2‑mercaptoethanol.

Abstract

The mode of action of aqueous garlic extract (AGE) was studied in Candida albicans. The minimum inhibitory concentration (MIC) of AGE against six clinical yeast isolates ranged between 0.8 and 1.6 mg ml−1. Scanning electron microscopy and cell leakage studies showed that garlic treatment affected the structure and integrity of the outer surface of the yeast cells. Growth of C. albicans in the presence of AGE affected the yeast lipid in a number of ways: the total lipid content was decreased; garlic-grown yeasts had a higher level of phosphatidylserines and a lower level of phosphatidylcholines; in addition to free sterols and sterol esters, C. albicans accumulated esterified steryl glycosides; the concentration of palmitic acid (16:0) and oleic acid (18:1) increased and that of linoleic acid (18:2) and linolenic acid (18:3) decreased. Oxygen consumption of AGE-treated C. albicans was also reduced. The anticandidal activity of AGE was antagonized by thiols such as L-cysteine, glutathione and 2-mercaptoethanol. Interaction studies between AGE and thiols included growth antagonism, enzymic inhibition and interference of two linear zones of inhibition. All three approaches suggest that AGE exerts its effect by the oxidation of thiol groups present in the essential proteins, causing inactivation of enzymes and subsequent microbial growth inhibition.

References

26