Multiple microbial and host protein thiols

Multiple microbial and host protein thiols refer to the sulfhydryl (-SH) groups found on cysteine residues within a wide array of proteins in both pathogens and human cells (Cremers & Jakob, 2013, PubMed). These thiols are essential for maintaining protein structure through disulfide bridges and are critical for the catalytic activity of numerous enzymes, particularly those involved in cellular respiration and metabolism (Lansdown, 2006, PubMed). In the context of pharmacology, these groups serve as a broad-spectrum target for various antiseptic and antimicrobial agents, such as silver ions and oxidizing compounds (Gottardi, 2001, StatPearls). When these agents interact with protein thiols, they cause protein denaturation, inactivation of essential enzymes, and loss of membrane integrity, ultimately leading to cell death (McDonnell & Russell, 1999, Clinical Microbiology Reviews). While highly effective against a diverse range of bacteria, fungi, and viruses, the lack of specificity means these agents can also affect host proteins, often limiting their use to topical applications (Lansdown, 2006, PubMed). Understanding the interaction between drugs and these thiol groups is vital for developing treatments for wound infections and managing oxidative stress-related conditions (Cremers & Jakob, 2013, PubMed).

Other names

Protein sulfhydryl groupsCysteine thiolsProtein-bound thiolsSulfhydryl groups

Drugs targeting these thiols typically act through covalent modification, oxidation, or metal coordination of the sulfhydryl (-SH) groups on cysteine residues (McDonnell & Russell, 1999, Clinical Microbiology Reviews). This interaction leads to the denaturation of structural proteins and the irreversible inhibition of metabolic enzymes, such as those in the electron transport chain (Lansdown, 2006, PubMed). For example, silver ions (Ag+) form stable silver-sulfur bonds, while oxidizing agents like iodine convert thiols into disulfides or sulfenic acids, disrupting the pathogen's cellular homeostasis (Gottardi, 2001, StatPearls).