Findings from large epidemiologic studies indicate that there is a link between smoking and extrinsic skin ageing. We previously reported that matrix metalloproteinases (MMPs) mediate connective tissue damage in skin exposed to tobacco smoke extracts. Tobacco smoke contains more than 3800 constituents, including numerous water-insoluble polycyclic aromatic hydrocarbons (PAHs) that trigger aryl hydrocarbon receptor (AhR) signalling pathways. To analyse the molecular mechanisms involved in tobacco smoke-induced skin ageing, we exposed primary human fibroblasts and keratinocytes to tobacco smoke extracts. Hexane- and water-soluble tobacco smoke extracts significantly induced MMP-1 mRNA in both human cultured fibroblasts and keratinocytes in a dose-dependent manner. To clarify the involvement of the AhR pathway, we used a stable AhR-knockdown HaCaT cell line. AhR knockdown abolished the increased transcription of the AhR-dependent genes CYP1A1/CYP1B1 and MMP-1 induced by either of the tobacco smoke extracts. Furthermore, the tobacco smoke extracts induced 7-ethoxyresorufin-O-deethylase activity, which was almost completely abolished by AhR knockdown. Likewise, treating fibroblasts with AhR pathway inhibitors, that is, the flavonoids 3-methoxy-4-nitroflavone and α-naphthoflavone, blocked the expression of CYP1B1 and MMP-1. These findings suggest that the tobacco smoke extracts induce MMP-1 expression in human fibroblasts and keratinocytes via activation of the AhR pathway. Thus, the AhR pathway may be pathogenetically involved in extrinsic skin ageing.

Native wood cellulose was oxidized by 2,2,6,6-tetramethylpiperidine-1-oxyl (TEMPO)-mediated oxidation, and the fibrous TEMPO-oxidized celluloses (TOCs) thus obtained were disintegrated in water to prepare TOC nanofibrils (TOCNs). The carboxyl groups of TOCs and TOCNs were methyl-esterified, and the methylated samples were dissolved in 8% LiCl/N,N-dimethylacetamide for size-exclusion chromatography/multiangle laser-light scattering (SEC-MALLS) analysis to obtain their molecular-mass (MM) values and MM distributions (MMDs). The results showed that remarkable depolymerization occurred in TOCs and TOCNs and depended on the oxidation and sonication conditions. Because single peaks without bimodal patterns were observed in the MMDs for all of the TOC and TOCN samples, depolymerization may have randomly occurred on whole cellulose molecules and oxidized cellulose molecules in the microfibrils during these treatments. Compared with the MM values obtained by SEC-MALLS, the intrinsic viscosities of TOCs dissolved in 0.5 M copper ethylenediamine solution provided lower MM values owing to depolymerization during the dissolution and postreduction processes.

We report the viscoelastic properties of core-shell-structured, hemicellulose-rich nanofibrillated cellulose (NFC) in dispersion and wet-film states. The hemicellulose-rich NFC (hemicellulose neutral sugars 23%, carboxylate 0.2 mmol g(-1)), prepared from Japanese persimmons, had a core crystallite thickness of 2.3 nm and unit fibril thickness of 4.2 nm. A carboxylate-rich NFC (hemicellulose neutral sugars 7%, carboxylate 0.9 mmol g(-1)) with crystallite and fibril widths of 2.5 and 3.3 nm, respectively, was used as a reference. The solid-concentration dependencies of the storage moduli of gel-like water dispersions of the hemicellulose-rich NFC were weaker than those of carboxylate-rich NFC, and the dispersions were loosely flocculated even at high salt concentrations and low pH values. The viscoelastic properties of wet NFC films were similar to those of their dispersions; the hemicellulose-rich NFC films were significantly less sensitive to salt concentration and pH and were soft and swollen at high salt concentrations and low pH values.

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