Nitric oxide-mediated regulation of the physiological and molecular responses induced by Ultraviolet-B (UV-B) radiation in plants

Previous studies have shown that ultraviolet B (UV-B) irradiation can stimulate biosynthesis of secondary metabolites. Several other studies have demonstrated that nitric oxide (NO) is an important signal molecule that plays a key role in plant defence responses to UV-B irradiation. However, the signalling mechanism of NO involvement in UV-B-induced secondary-metabolite synthesis is unclear. The purpose of the present study is to investigate the role of NO in the accumulation UV-B-induced secondary metabolite in the leaves of Ginkgo biloba. Our results showed that UV-B irradiation induced multiple biological responses in the leaves of G. biloba, including increases in both NO production and nitric oxide synthase (NOS) activity, and subsequent activation of phenylalanine ammoniumlyase (PAL) and synthesis of flavonoids. Application of NO via the donor sodium nitroprusside (SNP) enhanced UV-B-induced PAL activity and increased accumulation of flavonoids in G. biloba leaves. Both the NOS inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME) and the NO scavenger 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (c-PTIO) reduced the production of NO. Moreover, UV-B-induced increase in PAL activity and flavonoid accumulation were suppressed by L-NAME and c-PTIO. These findings suggest a causal relationship between NO release and both PAL activity and flavonoid accumulation under UV-B irradiation. In addition, the results also indicate that NO, produced via NOS-like activity in ginkgo leaves subjected to UV-B irradiation, might act as an essential signal molecule for triggering the activation of PAL and synthesis of flavonoids.

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Autologous nitric oxide protects mouse and human keratinocytes from ultraviolet B radiation-induced apoptosis

AJP Cell Physiology ◽

10.1152/ajpcell.00462.2002 ◽

2003 ◽

Vol 284 (5) ◽

pp. C1140-C1148 ◽

Cited By ~ 53

Author(s):

Richard Weller ◽

Ann Schwentker ◽

Timothy R. Billiar ◽

Yoram Vodovotz

Keyword(s):

Nitric Oxide ◽

Soluble Guanylate Cyclase ◽

Ultraviolet B ◽

Skin Damage ◽

Wild Type ◽

No Donor ◽

Ultraviolet B Radiation ◽

Inducible Nos

Nitric oxide (NO) can either prevent or promote apoptosis, depending on cell type. In the present study, we tested the hypothesis that NO suppresses ultraviolet B radiation (UVB)-induced keratinocyte apoptosis both in vitro and in vivo. Irradiation with UVB or addition of the NO synthase (NOS) inhibitor N G-nitro-l-arginine methyl ester (l-NAME) increased apoptosis in the human keratinocyte cell line CCD 1106 KERTr, and apoptosis was greater when the two agents were given in combination. Addition of the chemical NO donor S-nitroso- N-acetyl-penicillamine (SNAP) immediately after UVB completely abrogated the rise in apoptosis induced by l-NAME. An adenoviral vector expressing human inducible NOS (AdiNOS) also reduced keratinocyte death after UVB. Caspase-3 activity, an indicator of apoptosis, doubled in keratinocytes incubated with l-NAME compared with the inactive isomer, d-NAME, and was reduced by SNAP. Apoptosis was also increased on addition of 1,H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ), an inhibitor of soluble guanylate cyclase. Mice null for endothelial NOS (eNOS) exhibited significantly higher apoptosis than wild-type mice both in the dermis and epidermis, whereas mice null for inducible NOS (iNOS) exhibited more apoptosis than wild-type mice only in the dermis. These results demonstrate an antiapoptotic role for NO in keratinocytes, mediated by cGMP, and indicate an antiapoptotic role for both eNOS and iNOS in skin damage induced by UVB.

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