Surfactant lipid damage

FIGURE 31.10 Lipid damage potential of a number of surfactants determined by the ability of surfactant micelles to solubilize cholesterol and stearic acid. 

Pulmonary epithelial cells have been extensively characterized as the producers of pulmonary surfactant lipid and protein species and in their role in the repair of epithelial damage through increased cell proliferation and subsequent differentiation. It is also clear that a subpopulation of the respiratory epithelium is capable of uptake, accumulation, and metabolism of inhaled and systemic lipophilic substances (89). 

The absorption of drugs from the rectal [32] cavity has been studied in some detail. Muranishi et al. [34] have shown that a significant increase in the absorption and lymphatic uptake of soluble and colloidal macromolecules can be achieved by pretreating the rectal mucosal membrane with lipid-nonionic surfactant mixed micelles. They found no evidence of serious damage of the mucosal membrane. Davis [30] suggested that the vaginal cavity could be an effective delivery site for certain pharmaceuticals, such as calcitonin, used for the treatment of postmenopausal osteoporosis. 

Phospholipid that is the major component of Tung surfactant, and the syndrome caused by its deficiency Dipalmitoylphosphatidylcholine (DPPC, also called dipalmitoyllecithin, DPPL) is the major lipid component of lung surfactant. It is made and secreted by type II granular pneu-mocytes. Insufficient surfactant production causes respiratory distress syndrome, which can occur in preterm infants or adults whose surfactant-producing pneumocytes have been damaged or destroyed. 

Formulation additives used in topical drug or pesticide formulations can alter the stratum comeum barrier. Surfactants are least likely to be absorbed, but they can alter the lipid pathway by fluidization and delipidization of lipids, and proteins within the keratinocytes can become denatured. This is mostly likely associated with formulations containing anionic surfactants than non-ionic surfactants. Similar effects can be observed with solvents. Solvents can partition into the intercellular lipids, thereby changing membrane lipophilicity and barrier properties in the following order ether/acetone > DMSO > ethanol > water. Higher alcohols and oils do not damage the skin, but they can act as a depot for lipophilic drugs on the skin surface. The presence of water in several of these formulations can hydrate the skin. Skin occlusion with fabric or transdermal patches, creams, and ointments can increase epidermal hydration, which can increase permeability. 

Treatment with the surfactant is another way to break the barrier, as described earlier.10 The efficacy depends on each surfactant. Yang et al.15 suggested that some kinds of anionic surfactant, such as sodium dodecyl sulfate (SDS), affect not only the SC barrier, but also the nucleous layer of the epidermis. Fartasch demonstrated16 that the topical application of SDS caused cell damage to the nucleated cells of the epidermis and acetone treatment disrupted the lipid structure only in the SC. Thus, if one wants to investigate the effect of the disruption of the SC barrier function, tape stripping or acetone treatment would be better for the study. 

The basic function of a cleanser is to promote health and hygiene of skin by removing excess dirt, sebum, and bacteria from skin and promoting exfoliation. However, as explained earlier, cleanser surfactants also interact with SC proteins and lipids, causing damage to the SC barrier, leading to a net loss in SC hydration. 

It is clear that harsh surfactants have the potential to cause immediate alteration to SC proteins and lipids, and progressively increasing degrees of damage over time that can eventually result in a barrier breakdown. The first step toward mild cleansing is to minimize the damage potential of surfactants... 

Long-term surfactant damage to the SC lipid extends from the short-term effects resulting in cumulative loss of barrier function and lipid fluidity leading to profound dryness. The results of an assessment... 

SC. Surfactant interaction with lipids and proteins leads to a fundamental breakdown of biological processes that underpin skin health. Mild surfactants have lead to cleansers with significantly reduced drying and damaging potential but only within the last decade have truly moisturizing cleansers begun to emerge. 

Warner, R.R. Boissy, Y.L. Lilly, N.A. Spears, M.J. McKillop, K. Marshall, J.L. Stone, K.J. Water disrupts stratum corneum lipid lamellae damage is similar to surfactants. J. Invest. Dermatol. 1999, 113, 960-966. 

The polar, ionic and even non-ionic head-group interactions of lipid membranes and other surfactants, (as indeed for many polymers and polyelectrolyte intra-molecular interactions) and the associated curvature at interfaces formed by such assemblies will be dependent on dissolved gas in quite complicated ways. Fluctuating nanometric sized cavities at such surfaces will be at extremely high pressure, (P = 2y/r, y= surface tension, and r the radius) resulting in formation of H and OH radicals. The immediate formation of Cl radicals and consequent damage to phospholipids offers em explanation of exercise-induced immunosuppression (through excess lactic acid CO2 production), perhaps a clue to the aging process. 

In other words, to produce oily soil roll-up, the detergent must make the hber surface more hydrophilic [14], Thus, the removal of lipid soil from hair is dominated by the hydrophilicity of the fiber surface, and anything that can be done to make the hber surface more hydrophilic, such as bleaching or washing with anionic surfactants in water, should facilitate oily soil removal. This is one of the reasons damaged hair, which is generally more hydrophilic at the surface, is so sensitive to oil removal and often appears very dry after shampooing. 

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