Lipid delipidization, effect

Yes - Anesthetics abolish immobilized lipids. Their effects on particle distribution, enzyme kinetics and protein conformation are quivalent to the effects of delipidation, suggesting that anesthetics affect primarily lipid protein interactions (16,17). 

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. 

In contrast, other lipids were able to restore the catalytic activity of P-gp ATPase after delipidation. Unsaturated PC and PS were most effective. The observed ranking in restoration for head groups was PC > PE > PS > PI. A strong preference for unsaturated fluid lipids with low Tt values was seen. These lipids are also preferred by various other ATPases. 

The exact mechanism of action of moisturizers and emollients is still unknown. Theoretically, the improvement in the barrier function could be due to absorption of the moisturizer into the delipidized stratum corneum, acting as an effective barrier, as suggested in a study on the effect of petrolatum (Ghadially et al. 1992). Due to a better knowledge of the structural organization of the horny layer with corneocytes embedded in between lipid bilayers (ceramides, cholesterol and free fatty acids in approximately equal quantities), new emollients could be developed to supply the missing elements in the bilayer structure after acute or chronic irritant contact. However, applications of ceramides, linoleic acid and a variety of other fatty acids alone have been reported to actually delay barrier recovery in acetone-treated murine skin, despite the fact that these lipids are required for barrier homeostasis. The only treatments that allowed normal barrier recovery were applications of complete mixtures of ceramide, fatty acid and cholesterol, or pure cholesterol (Man et al. 

There is abundant evidence for the view that calcium translocation, as well as ATP hydrolysis, is mediated by a Ca " -ATPase situated in the sarcoplasmic reticulum membranes (MacLennan and Holland, 1975). Lipid dependency of both of these functions has also been known for some time. Treatment of membrane preparations or of the Ca -ATPase with phospholipases results in parallel loss of both functions, whereas the restoration of both follows phospholipid addition. In early studies, lecithin alone has been effective in restoring ATPase activity of the delipidated enzyme while, for calcium translocation, phosphatidyl-ethanolamine was required as well (MacLennan and Holland, 1976). 

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