Membrane changes under oxidative stress: the impact of oxidized lipids

Abstract

Studying photosensitized oxidation of unsaturated phospholipids is of importance for understanding the basic processes underlying photodynamic therapy, photoaging and many other biological dysfunctions. In this review we show that the giant unilamellar vesicle, when used as a simplified model of biological membranes, is a powerful tool to investigate how in situ photogenerated oxidative species impact the phospholipid bilayer. The extent of membrane damage can be modulated by choosing a specific photosensitizer (PS) which is activated by light irradiation and can react by either type I and or type II mechanism. We will show that type II PS generates only singlet oxygen which reacts to the phospholipid acyl double bond. The byproduct thus formed is a lipid hydroperoxide which accumulates in the membrane as a function of singlet oxygen production and induces an increase in its area without significantly affecting membrane permeability. The presence of a lipid hydroperoxide can also play an important role in the formation of the lipid domain for mimetic plasma membranes. Lipid hydroperoxides can be also transformed in shortened chain compounds, such as aldehydes and carboxylic acids, in the presence of a PS that reacts via the type I mechanism. The presence of such byproducts may form hydrophilic pores in the membrane for moderate oxidative stress or promote membrane disruption for massive oxidation. Our results provide a new tool to explore membrane response to an oxidative stress and may have implications in biological signaling of redox misbalance.

Mentha pulegium crude extracts induce thiol oxidation and potentiate hemolysis when associated to t-butyl hydroperoxide in human’s erythrocytes

“…Importantly, t-BHP does not induce hemolysis per se at saline ranging from 0.8% to 0.9%, and does not induced NPSH oxidation. Accordingly, we suggest that the t-BHP-induced damage to lipids (evaluated here as TBARS) weakens the membrane making cells more susceptible to hemolysis at lower saline, which are in accordance to literature (Trotta et al 1983, Itri et al 2014). In turn, we found here that t-BHP does not increase NPSH oxidation and methaemoglobin content (data not shown) under our experimental conditions, contrasting to previous data (Trotta et al 1983, Adesanoye et al 2013, Portela et al 2017.…”

Computational strategies for predicting free radical scavengers' protection against oxidative stress: Where are we and what might follow?

“…LOO • , and their nonradical partners lipid hydroperoxides (LOOH), can be transformed by enzymatic or nonenzymatic processes into other oxidation products including aldehydes, alkanes, and alkenes . these species represent a threat to membranes integrity, and can react with biologically relevant molecules (including proteins and DNA) leading to structural modifications that can ultimately cause cell death and genotoxicity …”

On thein vivophotochemical rate parameters for PDT reactive oxygen species modeling

“…The reactivity of 1 O 2 with biomolecules (e.g., membranes and lipids), amino acids (e.g., His, Trp, and Met), and nucleic acids (e.g., guanosine) as model systems to help in understanding the mechanism of toxiciy in PDT (Cadet et al , 2006; Girotti, 2001; Itri et al , 2014; McDonagh, 2001; Kanofsky, 1989). Reaction of 1 O 2 with methionine is an example of heteroatom oxidation in proteins (Fig.…”