Iron and iron chelators: a review on potential effects on skin aging.

Similar to oxygen, iron is essential for aerobic life and energy production. Akin to oxygen, iron can be toxic and accelerate the aging process. Indeed, via the Fenton and Haber Weiss reactions, iron potentiates the generation of highly reactive oxygen free radicals such as hydroxyl radical, thus stimulating oxidative damage.

The stratum corneum: a double paradox.

The stratum corneum (SC) (i.e., the outermost layer of human skin) is a complex and paradoxical tissue composed of corneocytes and a matrix of intercellular lipids playing an essential role as the skin's protective barrier.

Increased proteolysis of diphtheria toxin by human monocytes after heat shock: a subsidiary role for heat-shock protein 70 in antigen processing.

The expression of heat-shock proteins (hsp) increases after exposure to various stresses including elevated temperatures, oxidative injury, infection and inflammation. As molecular chaperones, hsp have been shown to participate in antigen processing and presentation, in part through increasing the stability and expression of major histocompatibility complex molecules. Heat shock selectively increases human T-cell responses to processed antigen, but does not affect T-cell proliferation induced by non-processed antigens.

Iron as the malignant spirit in successful ageing.

Iron enhances the production of the highly reactive and toxic hydroxyl radical, thus stimulating oxidative damage. Iron has been associated with a number of oxidative injury-dependent, age-related conditions and diseases. Indeed, oxidative injury is a major factor of (accelerated) ageing.

Effects of exogenous surfactant and recombinant human copper-zinc superoxide dismutase on oxygen-dependent antimicrobial defenses.

The use of human recombinant CuZn superoxide dismutase (rhSOD) in addition to exogenous surfactant has been studied as a therapeutic strategy to prevent acute and chronic lung injury in premature infants with blood monocytes (MO). However, scavenging of superoxide by rhSOD may compromise bacterial killing by phagocytes. In the present study, we investigated the interaction of exogenous surfactant and rhSOD with the antibacterial activity of human blood MO.

Toxicity of cadmium in tobacco smoke: protection by antioxidants and chelating resins.

The effects of cadmium, an environmental toxin present in tobacco smoke, were studied in vitro in human monocytes and compared to those of tobacco smoke. Overexpression of the 72kDa heat shock/stress protein Hsp70 and cell death occurred with a similar time-course and to a similar extent in human monocytes exposed to either cadmium or tobacco smoke. Cadmium and tobacco smoke-mediated toxicity were associated with a decrease in the cellular content of glutathione and ATP and the glutathione precursor N-acetyl-L-cysteine prevented both cadmium and tobacco smoke-mediated toxicity.

Hyperthermia assists survival of astrocytes from oxidative-mediated necrotic cell death.

In response to many stresses and pathologic states, including different models of nervous system injury, cells synthesize a variety of proteins, most notably the inducible 72 kDa heat shock protein 70 (Hsp70), which plays important roles in maintaining cellular integrity and viability. We report here that cultured astrocytes from rat diencephalon express high levels of Hsp70 upon exposure to elevated temperatures, and are less vulnerable to a subsequent oxidative stress. Complex oxidative stress was induced by exposure of astrocytes to an aqueous extract of tobacco smoke.

Mitochondrial membrane potential: a novel biomarker of oxidative environmental stress.

Epidemiologic analyses, traditionally based on long-term cohort or case-control studies, provide retrospective causal associations between exposure to a particular environmental stressor and an exposure-related disease end point. Recent research initiatives have propelled a shift toward exploring molecular epidemiology and molecular biological markers (biomarkers) as a means of providing more immediate, quantitative risk assessment of potentially deleterious environmental exposures. We compared, in normal human monocytes isolated from the blood of healthy donors, variations in Hsp70 expression and mitochondrial membrane potential (delta psi m) in response to exposure to either tobacco smoke or gamma-irradiation, two models for environmentally mediated oxidant exposure.

Mitochondrial alterations precede Bordetella pertussis-induced apoptosis.

Bordetella pertussis, the causative agent of whooping cough in humans, secretes a number of toxins, including adenylate cyclase-hemolysin (AC-Hly), and induces macrophage apoptosis. We investigated the effects of B. pertussis on mitochondrial membrane potential (deltapsim) and ATP levels, as possible determinants of cell death.