Protection against Ultraviolet A-Induced Skin Apoptosis and Carcinogenesis through the Oxidative Stress Reduction Effects of N-(4-bromophenethyl) Caffeamide, A Propolis Derivative.

Ultraviolet A (UVA) is a major factor in skin aging and damage. Antioxidative materials may ameliorate this UV damage. This study investigated the protective properties of N-(4-bromophenethyl) caffeamide (K36H) against UVA-induced skin inflammation, apoptosis and genotoxicity in keratinocytes. The protein expression or biofactor concentration related to UVA-induced skin damage were identified using an enzyme-linked immunosorbent assay and western blotting. K36H reduced UVA-induced intracellular reactive oxygen species generation and increased nuclear factor erythroid 2-related factor 2 translocation into the nucleus to upregulate the expression of heme oxygenase-1, an intrinsic antioxidant enzyme. K36H inhibited UVA-induced activation of extracellular-signal-regulated kinases and c-Jun N-terminal kinases, reduced the overexpression of matrix metalloproteinase (MMP)-1 and MMP-2 and elevated the expression of the metalloproteinase-1 tissue inhibitor. Moreover, K36H inhibited the phosphorylation of c-Jun and downregulated c-Fos expression. K36H attenuated UVA-induced Bax and caspase-3 expression and upregulated antiapoptotic protein B-cell lymphoma 2 expression. K36H reduced UVA-induced DNA damage. K36H also downregulated inducible nitric oxide synthase, cyclooxygenase-2 and interleukin-6 expression as well as the subsequent generation of prostaglandin E2 and nitric oxide. We observed that K36H ameliorated UVA-induced oxidative stress, inflammation, apoptosis and antiphotocarcinogenic activity. K36H can potentially be used for the development of antiphotodamage and antiphotocarcinogenic products.

1,2-Bis[(3-Methoxyphenyl)Methyl]Ethane-1,2-Dicarboxylic Acid Reduces UVB-Induced Photodamage In Vitro and In Vivo.

This study investigated the effects and mechanisms of 1,2-bis[(3-methoxyphenyl)methyl]ethane-1,2-dicarboxylic acid (S4), a sesamin derivative, on anti-inflammation and antiphotoaging in vitro and in vivo. Human skin fibroblasts were treated with S4 and did not show cytotoxicity under concentrations of 5-50 µM. In addition, S4 also reduced ultraviolet (UV)B-induced intracellular reactive oxygen species (ROS) production. Additionally, S4 inhibited UVB-induced phosphorylation of mitogen-activated protein (MAP) kinases, activator protein-1 (AP-1), and matrix metalloproteinases (MMPs) overexpression. Furthermore, S4 also inhibited UVB-induced Smad7 protein expression and elevated total collagen content in human dermal fibroblasts. For anti-inflammatory activity, S4 inhibited UVB-induced nitric oxide synthase (i-NOS) and cyclooxygenase (COX)-2 protein expression and inhibited nuclear factor-kappaB (NF-ĸB) translocation into the nucleus. S4 ameliorated UVB-induced erythema and wrinkle formation in hairless mice. On histological observation, S4 also ameliorated UVB-induced epidermal hyperplasia and collagen degradation. S4 reduced UVB-induced MMP-1, interleukin (IL)-6, and NF-ĸB expression in the mouse skin. The results indicated that S4 had antiphotoaging and anti-inflammatory activities, protecting skin from premature aging.

Protective Effects of Sesamin against UVB-Induced Skin Inflammation and Photodamage In Vitro and In Vivo.

Ultraviolet (UV) exposure has been demonstrated as the most critical factor causing extrinsic skin aging and inflammation. This study explored the protective effects and mechanisms of sesamin against skin photodamage. Sesamin reduced intracellular reactive oxygen species production after UVB irradiation in human dermal fibroblasts. The sesamin treatment attenuated mitogen-activated protein (MAP) kinase phosphorylation and matrix metalloproteinase (MMPs) overexpression induced by UVB exposure, and it significantly enhanced the tissue inhibitor of metalloproteinase-1 protein expression. Sesamin also elevated the total collagen content in human fibroblasts by inhibiting UVB-induced mothers against decapentaplegic homolog 7 (Smad7) protein expression. Sesamin reduced UVB-induced inducible nitric oxide synthase (i-NOS) and cyclooxygenase-2 (COX-2) overexpression and inhibited nuclear factor-kappa B (NF-κB) translocation. Moreover, sesamin may regulate the c-Jun N-terminal kinases (JNK) and p38 MAP kinase pathways, which inhibit COX-2 expression. Sesamin could reduce UVB-induced inflammation, epidermal hyperplasia, collagen degradation, and wrinkle formation in hairless mice. It also reduced MMP-1, interleukin (IL-1), i-NOS, and NF-κB in the mouse skin. These results demonstrate that sesamin had antiphotodamage and anti-inflammatory activities. Sesamin has potential for use as a skin protection agent in antiphotodamage and skin care products.

Sesamol Inhibited Ultraviolet Radiation-Induced Hyperpigmentation and Damage in C57BL/6 Mouse Skin.

Melanin is synthesized through a series of oxidative reactions initiated with tyrosine and catalyzed by melanogenesis-related proteins such as tyrosinase, tyrosinase-related protein-1 (TRP-1), dopachrome tautomerase (TRP-2), and microphthalmia-associated transcription factor (MITF). Our previous study demonstrated that sesamol inhibited melanin synthesis through the inhibition of the melanocortin 1 receptor (MC1R)/MITF/tyrosinase pathway in B16F10 cells. In this study, sesamol was applied to C57BL/6 mouse skin to understand its activity with respect to skin pigmentation. The results indicated that ultraviolet (UV) B-induced hyperpigmentation in the C57BL/6 mouse skin was significantly reduced by topical application of sesamol for 4 weeks. Sesamol reduced the melanin index and melanin content of the skin. In addition, sesamol elevated the brightness (L* value) of the skin. Sesamol also reduced UVB-induced hyperplasia of epidermis and collagen degradation in dermis. In immunohistochemical staining, topical application of sesamol reduced UVB-induced tyrosinase, TRP-1, TRP-2, and MITF expression in the epidermis of the skin. These results demonstrated that sesamol is a potent depigmenting agent in the animal model.

Protective Effects and Mechanisms of N-Phenethyl Caffeamide from UVA-Induced Skin Damage in Human Epidermal Keratinocytes through Nrf2/HO-1 Regulation.

The skin provides an effective barrier against physical, chemical, and microbial invasion; however, overexposure to ultraviolet (UV) radiation causes excessive cellular oxidative stress, which leads to skin damage, DNA damage, mutations, and skin cancer. This study investigated the protective effects of N-phenethyl caffeamide (K36) from UVA damage on human epidermal keratinocytes. We found that K36 reduced UVA-induced intracellular reactive oxygen species (ROS) production and induced the expression of the intrinsic antioxidant enzyme heme oxygenase-1 (HO-1) by increasing the translocation of nuclear factor erythroid 2⁻related factor 2 (Nrf2). K36 could inhibit the phosphorylation of extracellular-signal-regulated kinase (ERK) and c-Jun N-terminal kinases (JNK) and reduce UVA-induced matrix metalloproteinase (MMP)-1 and MMP-2 overexpression; it could also elevate the expression of tissue inhibitors of metalloproteinases (TIMP). In addition, K36 ameliorated 8-hydroxy-2'-deoxyguanosine (8-OHdG) induced by UVA irradiation. Furthermore, K36 could downregulate the expression of inducible nitric oxide synthase (iNOS) and interleukin-6 (IL-6) and the subsequent production of nitric oxide (NO) and prostaglandin E2 (PGE2). Based on our findings, K36 possessed potent antioxidant, anti-inflammatory, antiphotodamage, and even antiphotocarcinogenesis activities. Thus, K36 has the potential to be used to multifunctional skin care products and drugs.

Protective effects and mechanisms of Terminalia catappa L. methenolic extract on hydrogen-peroxide-induced oxidative stress in human skin fibroblasts.

BACKGROUND: Oxidative stress plays a crucial role in aging-related phenomenon, including skin aging and photoaging. This study investigated the protective role and possible mechanism of Terminalia catappa L. methanolic extract (TCE) in human fibroblasts (Hs68) against hydrogen peroxide (H2O2)-induced oxidative damage. METHODS: Various in vitro antioxidant assays were performed in this study. The effect and mechanisms of TCE on oxidative stress-induced oxidative damage were studied by using western blotting. RESULTS: The IC50 of TCE was 8.2 µg/mL for 1,1-diphenyl-2-picrylhydrazyl radical scavenging, 20.7 µg/mL for superoxide anion radical scavenging, 173.0 µg/mL for H2O2 scavenging, 44.8 µg/mL for hydroxyl radical scavenging, and 427.6 µg/mL for ferrous chelation activities. Moreover, TCE inhibited the H2O2-induced mitogen-activated protein kinase signaling pathway, resulting in the inhibition of c-Jun, c-Fos, matrix metalloproteinase (MMP)-1, MMP-3, MMP-9, and cyclooxygenase-2 expression. TCE also increased hemeoxygenase-1 expression inhibited by H2O2. Finally, TCE was demonstrated reverse type I procollagen expression in fibroblasts after H2O2 treatment. CONCLUSIONS: According to our findings, TCE is a potent antioxidant and protective agent that can be used in antioxidative stress-induced skin aging.

Sesamol Inhibited Melanogenesis by Regulating Melanin-Related Signal Transduction in B16F10 Cells.

Melanin is synthesized through a series of interactions catalyzed by melanogenic enzymes such as tyrosinase, dopachrome tautomerase (tyrosinase-related protein-2; TRP-2), and tyrosinase-related protein-1 (TRP-1). Tyrosinase plays a key role in catalysing the initial and limiting steps of melanogenesis. The melanin that results from melanogenesis has the protective effect of absorbing ultraviolet radiation. However, overproduction of melanin, in addition to altering the appearance of skin, may lead to skin disorders such as melasma, solar lentigo, and postinflammatory hyperpigmentation. Previous studies have revealed that sesamol is a strong antioxidant and a free radical scavenger. In this study, we investigated the effects of sesamol on the regulation of melanogenesis and related mechanisms in B16F10 cells. The results indicated that sesamol inhibited tyrosinase activity and melanogenesis induced by α-melanocyte-stimulating hormone (α-MSH) in B16F10 melanoma cells. Sesamol decreased the protein level of melanocortin 1 receptor (MC1R), microphthalmia-associated transcription factor (MITF), tyrosinase, and TRP-1 by downregulating cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) pathways that had been activated by α-MSH. Sesamol increased glycogen synthase kinase 3 beta (GSK3ß), protein kinase B (AKT), and extracellular signal-related kinase (ERK) phosphorylation, thus inhibiting the transcription of MITF. Sesamol also inhibited melanin synthesis and tyrosinase expression by modulating ERK, phosphoinositide 3-kinase (PI3K)/AKT, p38, and c-Jun amino-terminal kinase (JNK) signalling pathways. These results indicate that sesamol acted as a potent depigmenting agent.

N-(4-bromophenethyl) Caffeamide Protects Skin from UVB-Induced Inflammation Through MAPK/IL-6/NF-κB-Dependent Signaling in Human Skin Fibroblasts and Hairless Mouse Skin.

Long-term exposure to ultraviolet (UV) irradiation causes skin inflammation and aging. N-(4-bromophenethyl) caffeamide (K36H) possesses antioxidant and antimelanogenic properties. The present study investigated the effects of K36H on UVB-induced skin inflammation in human skin fibroblasts and hairless mice and evaluated the underlying mechanisms. The in vitro results indicated that K36H reduced UVB-induced mitogen-activated protein kinase (MAP kinase) expression. Furthermore, K36H treatment reduced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expression in UVB-irradiated fibroblasts by regulating IκB and nuclear factor-kappa B (NF-κB) expression. In the animal study, topically applied K36H markedly reduced inflammation and skin thickness and prevented photodamage to the skin of hairless mice. In addition, K36H inhibited the levels of UV-upregulated inflammation-related proteins levels such as IL-1, iNOS, and NF-κB in the dermis of hairless mice. Our findings demonstrated the antioxidant and anti-inflammatory properties of K36H in human skin fibroblasts and hairless mice. Therefore, K36H can be developed as an antiphotodamage and antiphotoinflammation agent.

Alleviation of Ultraviolet B-Induced Photodamage by Coffea arabica Extract in Human Skin Fibroblasts and Hairless Mouse Skin.

Coffea arabica extract (CAE) containing 48.3 ± 0.4 mg/g of chlorogenic acid and a trace amount of caffeic acid was found to alleviate photoaging activity in human skin fibroblasts. In this study, polyphenol-rich CAE was investigated for its antioxidant and antiinflammatory properties, as well as for its capability to alleviate ultraviolet B (UVB)-induced photodamage in BALB/c hairless mice. The results indicated that 500 µg/mL of CAE exhibited a reducing power of 94.7%, ferrous ion chelating activity of 46.4%, and hydroxyl radical scavenging activity of 20.3%. The CAE dose dependently reduced UVB-induced reactive oxygen species (ROS) generation in fibroblasts. Furthermore, CAE inhibited the UVB-induced expression of cyclooxygenase-2 and p-inhibitor κB, and the translocation of nuclear factor-kappa B (NF-κB) to the nucleus of fibroblasts. In addition, CAE alleviated UVB-induced photoaging and photodamage in BALB/c hairless mice by restoring the collagen content and reduced UVB-induced epidermal hyperplasia. CAE also inhibited UVB-induced NF-κB, interleukin-6, and matrix metalloproteinase-1 expression in the hairless mouse skin. The results indicated that CAE exhibits antiphotodamage activity by inhibiting UV-induced oxidative stress and inflammation. Therefore, CAE is a candidate for use in antioxidant, antiinflammatory, and antiphotodamage products.

N-(4-methoxyphenyl) caffeamide-induced melanogenesis inhibition mechanisms.

BACKGROUND: The derivative of caffeamide exhibits antioxidant and antityrosinase activity. The activity and mechanism of N-(4-methoxyphenyl) caffeamide (K36E) on melanogenesis was investigated. METHODS: B16F0 cells were treated with various concentrations of K36E; the melanin contents and related signal transduction were studied. Western blotting assay was applied to determine the protein expression, and spectrophotometry was performed to identify the tyrosinase activity and melanin content. RESULTS: Our results indicated that K36E reduced α-melanocyte-stimulating hormone (α-MSH)-induced melanin content and tyrosinase activity in B16F0 cells. In addition, K36E inhibited the expression of phospho-cyclic adenosine monophosphate (cAMP)-response element-binding protein, microphthalmia-associated transcription factor (MITF), tyrosinase, and tyrosinase-related protein-1 (TRP-1). K36E activated the phosphorylation of protein kinase B (AKT) and glycogen synthase kinase 3 beta (GSK3ß), leading to the inhibition of MITF transcription activity. K36E attenuated α-MSH induced cAMP pathways, contributing to hypopigmentation. CONCLUSIONS: K36E regulated melanin synthesis through reducing the expression of downstream proteins including p-CREB, p-AKT, p-GSK3ß, tyrosinase, and TRP-1, and activated the transcription factor, MITF. K36E may have the potential to be developed as a skin whitening agent.

Anti-Inflammatory and Anticancer Activities of Taiwanese Purple-Fleshed Sweet Potatoes (Ipomoea batatas L. Lam) Extracts.

Purple-fleshed sweet potato (PFSP) (Ipomoea batatas L. Lam) has been known to possess high amount of anthocyanins which contribute to its antioxidant activity. However, a few reports are available concerning its anti-inflammatory and anticancer properties. In this study, PFSP "Tainung 73," which is locally grown in Taiwan, was steamed and extracted using acidified ethanol pH 3.5 under 80°C. Two kinds of crude anthocyanins extracts were obtained, namely, SP (Steamed, Peeled) and SNP (Steamed, No Peeled). Then, anti-inflammatory and anticancer activities of these extracts were investigated. Cell viability assay (MTT) showed that SP and SNP extracts were not toxic to RAW 264.7 cells. They even exhibited anti-inflammatory activities by suppressing the production of NO and proinflammatory cytokines, such as NF-κß, TNF-α, and IL-6, in LPS-induced macrophage cells. Anticancer activities of these extracts were displayed through their ability to inhibit the growth of cancer cell lines, such as MCF-7 (breast cancer), SNU-1 (gastric cancer), and WiDr (colon adenocarcinoma), in concentration- and time-dependent manner. Further studies also revealed that SP extracts could induce apoptosis in MCF-7 and SNU-1 cancer cells through extrinsic and intrinsic pathway. In the future, PSFP extracts may have potential to be applied in nutraceutical, pharmaceutical, and food industries.

The optimum submerged culture condition of the culinary-medicinal white jelly mushroom (Tremellomycetes) and its antioxidant properties.

Tremella fuciformis is a natural edible and medicinal mushroom commercially available in Taiwan. In this study, the effects of initial pH, incubation time, and various media to optimize exopolysaccharide (EPS) production by T. fuciformis were evaluated in shake flasks and a bioreactor. The antioxidant properties were investigated. The results showed that using potato dextrose broth medium (pH 9) and a 48-hour incubation time in a shake flask was the most efficient condition from which to obtain maximum EPS. However, the quantity of EPS from different initial pH values (5-9) was not significantly different. Total polyphenol and ß-glucan contents from every EPS sample (pH 5-9) were evaluated. T. fuciformis polysaccharides (10 mg/mL, pH 9) could scavenge 40.63% of 1,1-diphenyl-2-picrylhydrazyl radicals. The chelating abilities of ferrous ion of all extracts reached more than 80%. EPS extract from the initial pH value of 9 showed the highest reducing power among the other pH values (half maximal effective concentration = 5.97 mg/mL). The EPS from T. fuciformis was noncytotoxic to mouse skin fibroblasts (NIH/3T3), and survival rates were more than 100% using MTT assay. The samples were used to analyze the scavenging activity against oxidative damage induced by ultraviolet B radiation and hydrogen peroxide. The results showed the antioxidant activity occurred in a dose-dependent manner (P < 0.05). Furthermore, these findings prove that the EPS of T. fuciformis from submerged culture possess antioxidant properties and can be used as an alternative treatment for cell protection.

The impact of polymorphisms in STAT6 on treatment outcome in HCV infected Taiwanese Chinese.

Genetic polymorphisms observed in various disease states associated with sensitivity or resistance to specific treatments have been a robust area of investigation for decades, with the potential to allow clinicians to make evidence-based decisions on the appropriate course of treatment. This study aimed to evaluate whether genetic polymorphisms of the signal transducer and activator of transcription 6 gene (STAT6) could be associated with a sustained virological response (SVR) among patients infected with hepatitis C virus genotypes 1 and 2 (HCV-1 and HCV-2) who were treated with peginterferon plus ribavirin (PEG-IFNα-RBV). We analyzed the associations between SVR to PEG-IFNα-RBV therapy and 4 single nucleotide polymorphisms (SNPs) in STAT6. This study included Taiwanese Chinese patients infected with either HCV-1 (n = 265) or HCV-2 (n = 195) in the presence or absence of an SVR. Among the STAT6 SNPs examined, the dosage effect of the A allele and allele frequency in rs1059513 were inversely correlated with SVR in patients infected with HCV-1 (P = 0.0179 and P = 0.0235, respectively). This effect was not observed in patients infected with HCV-2. The GG, GGG, and GGGC STAT6 haplotypes comprising 2, 3, and 4 SNPs (rs1059513, rs703817, rs324015, and rs3024974) were found to be associated with SVR, and their presence may increase the probability of a successful treatment outcome in patients infected with HCV-1 (P = 0.0273, 0.0352, and 0.0368, respectively). Moreover, a multivariate logistic regression model for predicting an SVR revealed that the presence of the GGGC haplotype carriers mutually affected the outcome of PEG-IFNα-RBV treatment. The presence of STAT6 SNPs and the association with SVR demonstrated that STAT6 polymorphisms might influence the therapeutic outcomes of patients infected with HCV-1 under standard-of-care (SOC) treatment.

Crude extracts of Agaricus brasiliensis induce apoptosis in human oral cancer CAL 27 cells through a mitochondria-dependent pathway.

In Taiwan, oral cancer is the fourth leading cause of male cancer mortality, and is still increasing. The Basiodiomycete, Agaricus brasiliensis Murill (ABM) is a dietary mushroom and has been known for its immuneenhancing, antitumor, antioxidation, antiviral and antimutagenesis functions. However, the exact anticancer mechanisms of ABM on human oral cancer cells are still unclear. In the present study, we investigated the effects of 50% ethanol crude extracts and hot water extracts of ABM on oral cancer CAL 27 cells. We observed that 0.9 mg/ml and 0.7 mg/ml of ABM 50% ethanol crude extracts and hot water, respectively, caused morphological changes and significantly reduced cell viability after 48-h treatment. The results showed that both extracts of ABM inhibited cell proliferation, increased the Ca(2+) release, reduced the mitochondria membrane potential (ΔΨm), and caused cell cycle arrest in the G(0)/G(1) phase, which contributed to apoptosis. Additionally, ABM induced DNA fragmentation, a characteristic of apoptosis and the expressions of apoptosis-related proteins, including apoptosis-inducing factor, cytochrome c, and caspase-3, were increased. Overall, we demonstrated that 50% ethanol crude extract and hot water extracts of ABM were able to induce apoptotic cell death in CAL 27 cells via the release of cytochrome c from mitochondria into the cytoplasm and activation of caspase-3 in vitro.

Control of silverleaf whitefly, cotton aphid and kanzawa spider mite with oil and extracts from seeds of sugar apple.

Development of alternative methods for pest management is needed with the increased concern for adverse effects of pesticides for human health and the environment. The main goal of our study was to test the oil from seeds of sugar apple (Annona squamosa), an edible tropical fruit for pest control. The oil pressed out of seeds was as effective in controlling the silverleaf whitefly, Bemisia argentifolii Bellows & Perring (Homoptera: Aleyrodidae), infesting leaves of tomato plants in greenhouse conditions as the recommended insecticide, with the advantage of not being phytotoxic. When observed with a scanning electron microscope, the seed oil caused whitefly nymphs to shrink and detach from the leaf surface. Sugar apple seed oil was also very effective in controlling the cotton aphid, Aphis gossypii Glover (Homoptera: Aphididae), on melon leaves and the Kanzawa spider mite, Tetranychus kanzawai Kishida (Acari: Tetranychidae), on soybean leaves. The study revealed the possibility of developing the oil from sugar apple seeds, an agricultural waste, into a broad spectrum product friendly to the environment and human health for crop pest management.

Control of silverleaf whitefly, cotton aphid and kanzawa spider mite with oil and extracts from seeds of sugar apple / Controle da mosca-branca, do pulgão do algodoeiro e do ácaro de kanzawa com óleo e extratos de sementes de fruta-do-conde

Development of alternative methods for pest management is needed with the increased concern for adverse effects of pesticides for human health and the environment. The main goal of our study was to test the oil from seeds of sugar apple (Annona squamosa), an edible tropical fruit for pest control. The oil pressed out of seeds was as effective in controlling the silverleaf whitefly, Bemisia argentifolii Bellows & Perring (Homoptera: Aleyrodidae), infesting leaves of tomato plants in greenhouse conditions as the recommended insecticide, with the advantage of not being phytotoxic. When observed with a scanning electron microscope, the seed oil caused whitefly nymphs to shrink and detach from the leaf surface. Sugar apple seed oil was also very effective in controlling the cotton aphid, Aphis gossypii Glover (Homoptera: Aphididae), on melon leaves and the Kanzawa spider mite, Tetranychus kanzawai Kishida (Acari: Tetranychidae), on soybean leaves. The study revealed the possibility of developing the oil from sugar apple seeds, an agricultural waste, into a broad spectrum product friendly to the environment and human health for crop pest management.

É crescente a necessidade de desenvolvimento de métodos alternativos para o manejo de pragas com o aumento da consciência pública sobre os efeitos adversos de pesticidas à saúde humana e ao ambiente. O objetivo principal deste trabalho foi o de avaliar o óleo de sementes de fruta-do-conde (Annona squamosa), uma fruta tropical comestível, para o controle de pragas. O óleo prensado de sementes foi tão eficiente quanto o pesticida recomendado para controle da mosca-branca Bemisia argentifolii Bellows & Perring (Homoptera: Aleyrodidae) infestando folhas de tomate em casa-de-vegetação, com a vantagem de não apresentar fitotoxicidade. Em observações ao microscópio eletrônico de varredura, o óleo de semente induziu ao ressecamento das ninfas e o seu desprendimento da superfície da folha. O óleo de sementes de fruta-do-conde também foi eficaz no controle do pulgão do algodoeiro, Aphis gossypii Glover (Homoptera: Aphididae), infestando folhas de melão, e do ácaro de Kanzawa, Tetranychus kanzawai Kishida (Acari: Tetranychidae), em folhas de soja. Este estudo revelou a possibilidade de utilizar o óleo de sementes de fruta-do-conde, um sub-produto agrícola, como produto de largo espectro de ação mas seguro ao ambiente e à saúde humana, em programas de manejo de pragas agrícolas.

Field Evaluation of Transgenic Papaya Lines Carrying the Coat Protein Gene of Papaya ringspot virus in Taiwan.

Four transgenic papaya lines expressing the coat protein (CP) gene of Papaya ringspot virus (PRSV) were evaluated under field conditions for their reaction to PRSV infection and fruit production in 1996 to 1999. Plants were exposed to natural virus inoculation by aphids in two adjacent fields in four different plantings at the same sites. None of the transgenic lines showed severe symptoms of PRSV whereas control nontransgenic plants were 100% severely infected 3 to 5 months after planting. In the first and second trials, 20 to 30% of the transgenic plants showed mild symptoms consisting of confined mottling or chlorotic spots on leaves. The number of transgenic plants with mild symptoms fluctuated according to the season and weather conditions, with a tendency to increase in the winter or rainy season and decrease in the summer. Also, the incidence of the mild symptoms in the third trial increased significantly due to infection by root rot fungi during the rainy season. Interestingly, there was no apparent adverse effect on fruit yield and quality in transgenic plants with mild symptoms. In the first and second experiments, transgenic lines yielded 10.8 to 11.6 and 54.3 to 56.7 times more marketable fruit, respectively, than controls. All transgenic plants produced fruit of marketable quality with no ringspots or distortion.