PREMIUM ANTI-BACTERIAL Q49 HAND WASH

Indications

• Antibacterial agent in personal care products
• Antiseptic in surgical settings
• Preservative in household products

Dosage

Children: For pediatric dosing, consult the BNF for Children, as specific dosages may vary based on the formulation and intended use.

Adults: Triclosan is typically used topically in various formulations. For specific dosing guidelines, refer to the product labeling or consult the BNF.

Mechanism of action

Triclosan exerts its antibacterial effects mainly by inhibiting fatty acid synthesis in bacteria. It binds to the enoyl-acyl carrier protein reductase enzyme (ENR), forming a ternary complex with NAD+. This complex cannot participate in fatty acid synthesis, leading to weakened cell membranes and ultimately cell death. Human cells are not affected as they do not possess the ENR enzyme.

Pharmacodynamics

Triclosan displays bacteriostatic activity at lower concentrations, inhibiting the growth and reproduction of bacteria. At higher concentrations, it exhibits bactericidal properties. The impact of triclosan on fatty acid metabolism is significant, as it disrupts essential lipid biosynthesis, which is crucial for maintaining bacterial cell structure and function. Additionally, triclosan has been associated with various biological effects, including potential endocrine disruption and reproductive toxicity.

Pharmacokinetics

Triclosan is generally poorly absorbed through the skin, but it can accumulate in human tissues and the environment. It is subject to metabolic processing, primarily in the liver, and is excreted through urine. The half-life of triclosan in humans varies, but it is typically around 24 hours. Environmental exposure pathways and its accumulation in aquatic organisms raise concerns regarding its ecological impact.

Adverse effects

• Skin irritation
• Allergic reactions
• Endocrine disruption
• Potential reproductive toxicity

Precautions

• Should be used with caution in individuals with a history of skin sensitivity
• Not recommended for prolonged use due to potential for skin irritation
• Avoid use in pregnant women due to potential reproductive effects

Pregnancy

Triclosan should be avoided during pregnancy due to potential adverse effects on fetal development.

Breast-feeding

Caution is advised when using triclosan while breastfeeding due to potential transfer through breast milk.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Topical creams
• Soaps
• Toothpastes
• Disinfectant solutions

Mechanism of action

Triclosan is a biocidal compound with multiple targets in the cytoplasm and membrane. At lower concentrations, however, triclosan appears bacteriostatic and is seen to target bacteria mainly by inhibiting fatty acid synthesis. Triclosan binds to enoyl-acyl carrier protein reductase enzyme (ENR). This complex has increased affinity for NAD+ and forms a ternary complex. This complex is unable to participate in fatty acid synthesis, weakening the cell membrane and causing cell death. Humans do not have an ENR enzyme, and thus are not affected. Triclosan (TCS) exposure has widely adverse biological effects such as influencing biological reproduction and endocrine disorders. While some studies have addressed TCS-induced expression changes of miRNAs and their related down-stream target genes, no data are available concerning how TCS impairs miRNA expression leading us to study up-stream regulating mechanisms. Four miRNAs (miR-125b, miR-205, miR-142a and miR-203a) showed differential expression between TCS-exposure treatments and the control group; their functions mainly involved fatty acid synthesis and metabolism. TCS exposure led to the up-regulation of mature miR-125b that was concomitant with consistent changes in pri-mir-125b-1 and pri-mir-125b-3 among its 3 pri-mir-125bs. Up-regulation of miR-125b originated from direct shear processes involving the two up-regulated precursors, but not pri-mir-125b2. Increased expression of pri-mir-125b-1 and pri-mir-125b-3 resulted from nfe2l2- and c/ebpa-integration with positive control elements of promoters for the two precursors. The overexpression of transcriptional factors, nfe2l2 and c/ebpa, initiated the promoter activity for the miR-125b precursor. CpG islands and Nfe2l2 were involved in constitutive expression of mir-125b-1 and mir-125b-3. The activities of two promoter regions, -487 to -1bp for pri-mir-125b1 and -1327 to +14bp for pri-mir-125b-3 having binding sites for NFE2 and Nfe2l2/MAF:NFE2, were higher than other regions, further demonstrating that the transcriptional factor Nfe2l2 was involved in the regulation of pri-mir-125b1 and pri-mir-125b-3. TCS's estrogen activity resulted from its effects on GPER, a novel membrane receptor, rather than the classical ERa and ERbeta. These results explain, to some extent, the up-stream mechanism for miR-125b up-regulation, and also provide a guidance to future mechanistic study on TCS-exposure.