Environmental stresses lower the efficiency of photosynthesis and sometimes cause irreversible damage to plant functions. When spinach thylakoids and Photosystem II membranes were illuminated with excessive visible light (100–1,000 µmol photons m−1 s−1) for 10 min at either 20°C or 30°C, the optimum quantum yield of Photosystem II decreased as the light intensity and temperature increased. Reactive oxygen species and endogenous cationic radicals produced through a photochemical reaction at and/or near the reaction center have been implicated in the damage to the D1 protein. Here we present evidence that lipid peroxidation induced by the illumination is involved in the damage to the D1 protein and the subunits of the light-harvesting complex of Photosystem II. This is reasoned from the results that considerable lipid peroxidation occurred in the thylakoids in the light, and that lipoxygenase externally added in the dark induced inhibition of Photosystem II activity in the thylakoids, production of singlet oxygen, which was monitored by electron paramagnetic resonance spin trapping, and damage to the D1 protein, in parallel with lipid peroxidation. Modification of the subunits of the light-harvesting complex of Photosystem II by malondialdehyde as well as oxidation of the subunits was also observed. We suggest that mainly singlet oxygen formed through lipid peroxidation under light stress participates in damaging the Photosystem II subunits.
The stratum corneum (SC) consists of corneocytes surrounded by a neutral lipid-enriched intercellular matrix. Ceramides represent approximately 50% of intercellular lipids, and play important roles in retaining epidermal water. The SC also contains covalently bound ceramides, which are thought to play a crucial role in the formation of lamellar structures, and are involved in maintaining skin barrier function. A previous report showed that levels of free ceramides in human SC changed with the seasons and age, although whether the content of different species of covalently bound ceramides also underwent such temporal changes was unclear. Here, SC samples were taken from 99 healthy individuals of different ages (24-64 years) and during different seasons. The content of different molecular species of covalently bound ceramides in the samples was quantified using HPLC-MS/MS. The levels of total covalently bound ceramides (Total-Cers) significantly decreased approximately 50% in autumn and winter, compared with that of spring and summer. The levels of covalently bound ceramides containing saturated fatty acids (SFA-Cers) in the spring and summer were approximately 2.3-fold higher than that seen in autumn and winter, whereas the level of covalently bound ceramides containing unsaturated fatty acids (USFA-Cers) in spring and summer were approximately 1.6-fold higher than that in autumn and winter. Furthermore, the ratio between SFA-Cers and USFA-Cers was significantly lower in spring and summer than in autumn and winter. The levels of SFA-Cers, but not USFA-Cers, were significantly lower in individuals ≥ 50 years old compared to those who are 30- and 40-years old in the spring. Our study showed for the first time that, similar to free ceramides, the level of covalently bound ceramides changed with the seasons. However, age-related changes in covalently bound ceramide content were limited in that only the amount of SFA-Cers in the spring was lower in older individuals.
Environmental stresses lower the efficiency of photosynthesis and sometimes cause irreversible damage to plant functions. When spinach thylakoids and Photosystem II membranes were illuminated with excessive visible light (100-1,000 mmol photons m 21 s 21 ) for 10 min at either 20uC or 30uC, the optimum quantum yield of Photosystem II decreased as the light intensity and temperature increased. Reactive oxygen species and endogenous cationic radicals produced through a photochemical reaction at and/or near the reaction center have been implicated in the damage to the D1 protein. Here we present evidence that lipid peroxidation induced by the illumination is involved in the damage to the D1 protein and the subunits of the light-harvesting complex of Photosystem II. This is reasoned from the results that considerable lipid peroxidation occurred in the thylakoids in the light, and that lipoxygenase externally added in the dark induced inhibition of Photosystem II activity in the thylakoids, production of singlet oxygen, which was monitored by electron paramagnetic resonance spin trapping, and damage to the D1 protein, in parallel with lipid peroxidation. Modification of the subunits of the light-harvesting complex of Photosystem II by malondialdehyde as well as oxidation of the subunits was also observed. We suggest that mainly singlet oxygen formed through lipid peroxidation under light stress participates in damaging the Photosystem II subunits.
Ceramides (Cers) are major constituents of the stratum corneum intercellular lipids, which are involved in the barrier function of the skin. Here, we examined the ratio of molecular species of Cers and their correlation with disease severity in patients with atopic dermatitis (AD). The levels of unsaturated fatty acids (USFAs) in both covalently bound and free Cers were higher in the lesional skin of patients with AD than in the non-lesional skin of patients with AD and normal skin of healthy controls. The proportion of USFAs (C30:1, C32:1, and C34:1) was considerably higher than that of other Cer molecular species in both covalently bound and free Cers in patients with AD. The proportion of USFAs in covalently bound Cers positively correlated with the levels of transepidermal water loss (TEWL) (r = 0.542) in the lesional skin of patients with AD. Additionally, the proportion of USFAs in covalently bound Cers positively correlated with thymus and activation-regulated chemokine (TARC), which is an index of disease severity, in the non-lesional (r = 0.676) and lesional (r = 0.503) skin of patients with AD. The proportion of USFA (C32:1), which was the highest in covalently bound Cers, also positively correlated with the TARC level in non-lesional (r = 0.733) and lesional (r = 0.515) skin of patients with AD. Our study is the first to show that there is an increase in USFA in not only lesional but also non-lesional skin of patients with AD. Moreover, this increase in USFA was associated with dryness and impaired barrier function and correlated with the TARC levels, a marker for the degree of type 2 inflammation. We speculate that exacerbation of type 2 inflammation may lead to abnormal epidermal lipid metabolism in the skin of patients with AD.
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