Effect of dietary omega-3 and omega-6 fatty acid sources on PUVA-induced cutaneous toxicity and tumorigenesis in the hairless mouse

Because of concern about psoralen-induced phototoxicity and photocarcinogenesis, we investigated the effects of dietary lipids in a mouse model in which 8-methoxypsoralen (8-MOP) and UVA (PUVA) therapy has been shown to be carcinogenic. SKH-Hr-1 hairless albino mice were fed diets containing either omega-3 or omega-6 fatty-acid sources (menhaden oil and corn oil, respectively). After 2 weeks on the diets, the mice were treated topically with 8-MOP and then exposed to UVA (5 J/cm²). Mice receiving the omega-3 fatty-acid source exhibited a marked decrease in inflammatory response and a more rapid repair, as expressed both grossly and microscopically. In support of the latter response, i.e. repair, ornithine decarboxylase activity was about 20% greater in animals receiving the omega-3 fatty-acid source. The effects of the dietary fatty acid sources on PUVA tumorigenesis were examined in long-term studies in which animals were treated topically with 0.01% 8-MOP thrice weekly after which they were exposed to UVA (1 J/cm²). These studies indicated that a dietary lipid rich in omega-3 fatty acid and known to exhibit anti-inflammatory properties can markedly ameliorate the course of PUVA toxicity but does not impede the course of PUVA tumorigenesis     

Photosensitivity induced by lomefloxacin versus other fluoroquinolones: A meta-analysis

Lomefloxacin may be more likely than other fluoroquinolones to cause photosensitivity. However, the rate of photosensitivity is variable and a meta-analysis has yet to be performed. The aim of this meta-analysis is to compare the rate of photosensitivity between outpatients who received lomefloxacin and those who received other fluoroquinolones. PubMed, EMBASE, Cochrane Library databases and trial registries were searched for randomized controlled trials (RCTs) of outpatients through June 12, 2019. The study outcome was the rate of photosensitivity based on the intention-to-treat principle, estimated by risk difference (RD) as the primary analysis and Peto odds ratio (Peto OR) as the secondary analysis, with 95% confidence intervals (CIs) using random-effects models. Four RCTs (total of 2295 patients) were included in this meta-analysis. A statistically higher risk of photosensitivity was found with lomefloxacin than with other fluoroquinolones (RD, 3.4%; 95% CI, 0.7%–6.2%; P-value = 0.013; I² = 10.9%). The odds of photosensitivity was also significantly higher with lomefloxacin (Peto OR, 5.81; 95% CI, 3.34 to 10.11; P-value <0.001; I² = 0%). This meta-analysis of RCTs found significantly higher photosensitivity with lomefloxacin compared to other fluoroquinolones. Considering this finding and given its lack of additional efficacy compared to other fluoroquinolones, lomefloxacin as a fluoroquinolone option should potentially be reconsidered.     

α-三噻吩对白纹伊蚊幼虫的毒杀作用

目的　研究α三噻吩对白纹伊蚊幼虫的杀灭效果、影响因素及其对白纹伊蚊幼虫生长发育的影响。　方法　在实验室特定近紫外光 (UVA)下,计数不同药物浓度、不同黑暗处理时间的α三噻吩作用后蚊幼虫的死亡数、化蛹数及蛹的羽化数;在户外自然光下,观测不同药物浓度、不同施药时间的α三噻吩作用后蚊幼虫的死亡数。　结果　实验室特定UVA下,α 三噻吩对白纹伊蚊幼虫的半数致死量为2.37μg/L;药物与幼虫在黑暗中作用3h后再施以UVA照射能发挥其最大毒杀作用;α三噻吩能够显著抑制白纹伊蚊幼虫的发育和蛹的羽化。户外自然光下,高浓度α 三噻吩在强烈阳光辐射下可以快速杀灭白纹伊蚊幼虫,上午5时施药后24h的毒杀作用显著优于上午10时和下午1时。　结论α三噻吩是一种高效、实用、并能够抑制蚊幼虫生长发育的杀虫剂。     

Comparative evaluation of cytotoxicity and phototoxicity of mono and diacylglycerol amino acid-based surfactants

Extensive efforts have been made, recently, to find surfactants with lower irritancy potential than those presently commercially employed in pharmaceutical and cosmetic preparations. Cytotoxic and phototoxic effects of novel mono and diacylglycerol amino acid-based surfactants (glutamic acid, or arginine) were evaluated.All tested surfactants showed a clear concentration–response relationship to two immortalized cell lines, murine fibroblast cell line, 3T3, and one human keratinocyte cell line, HaCaT, demonstrated by and decrease of NR uptake. Concentrations resulting in 50% inhibition of NR uptake (IC₅₀) range from 30 to 300 μg mL⁻¹.The potential phototoxicity which could result in irritant products, was determined by modulated cytotoxicity via the resazurin reduction to resorufin and neutral red uptake (NRU) endpoints. Surfactants with two chains showed, in general, less cytotoxic but higher phototoxic effect than surfactants with only one chain.     

Predicting petroleum phototoxicity

Phototoxicity to Daphnia magna was studied on 14 polycyclic aromatic hydrocarbons (PAHs) and 22 petroleum products (ranging from diesel to crude oil). The phototoxicity ranking of pure PAHs was about the same as found in another study on fish gill cells in vitro (Toxicology 127 (1998) 143), suggesting that the relative acute phototoxicity does not differ significantly between different species. Most petroleum products were found to be phototoxic, although the results differ somewhat between test methods (preparation of water-accommodated fractions or petroleum ether dissolved oil slurries). The degree of phototoxicity of a sample is related to both the source and the refining process of the crude oil. The best chemical predictors found were the concentrations of eight phototoxic parent PAHs. An even simpler analytical technique suggested for initial screening would be direct measurements of "total PAH," where samples having more than 3% PAH should be studied further.     

二苯甲酮类防晒剂的结构和安全性研究

目的 通过对二苯甲酮3种衍生物二苯甲酮-1、二苯甲酮-2和二苯甲酮-3进行皮肤光毒实验和皮肤光变态反应,探讨3种不同结构防晒剂对皮肤的安全性.方法 用HyperChem7.0软件分别计算出上3种防晒剂的总能量、结合能、电子能、净电荷、偶极矩等结构参数,用SPSS13.0软件分析不同结构参数和防晒剂皮肤光毒反应指数及光变态反应指数的相关性.结果 光毒反应指数和结构参数中的总能量和电子能呈负相关(P<0.01),并随净电荷之和的增加而上升(P<0.01).光变态反应指数仅和结构参数中的结合能密切相关(P<0.01),和其他结构参数均无相关性(P>0.05).结论 初步确定光毒反应指数和结构总能量、电子能相关.光变态反应指数和结合能相关.从而初步建立结构总能量、电子能、净电荷之和-皮肤光毒反应模型以及结合能-光变态反应模型.     

Voriconazole-induced photosensitivity

Voriconazole is a broad-spectrum triazole antifungal agent indicated for invasive aspergillosis, refractory Candida infections, and other emerging invasive fungal infections. Adverse cutaneous reactions associated with voriconazole therapy occur in fewer than 10% of treated patients and range from mild erythematous eruptions to life-threatening reactions such as the Stevens-Johnson syndrome and toxic epidermal necrolysis. Photosensitivity reactions are an uncommon but characteristic dermatitis in voriconazole recipients, particularly following chronic administration. We report a case of voriconazole-induced phototoxicity in a 50-year-old male with Candida parapsilosis endocarditis that reversed on discontinuation of the drug.     

Ketoprofen: experimental overview of dermal toxicity

Ketoprofen (KP) is a widely used non-steroidal anti-inflammatory drug (NSAID). However, an increasing number of case reports suggest that in broad use, KP can cause allergic dermatitis. Most of these adverse effects have been attributed to the photoallergic potential of KP and photosensitivity. With the exception of a few reports in experimental animals, there is little evidence that KP actually causes dermal toxicity. In this study, in order to investigate the eventual underlying causes of KP dermal toxicity, we conducted primary irritation, skin cumulative, skin sensitization, phototoxicity and photosensitization tests in rodents and rabbits. Primary irritation and skin cumulative testing using New Zealand white rabbits revealed that application of KP (22, 15 and 10%) did not induce erythema or edema formation. Moreover, in skin sensitization and skin phototoxicity testing, using Hartley albino guinea pigs, there was no evidence of allergic or phototoxic potential. In the photosensitization test, KP induced skin reactions in six of eight guinea pigs with signs of erythema on the application site. Histologically, in photosensitized skin, epidermal hyperplasia, including incremental stratum granulosum, acanthosis, keratinocyte hypertrophy and dermal inflammatory cell infiltration, was observed. In this animal study, no primary irritation, cumulative irritation, skin sensitization or skin phototoxicity was observed with KP treatment. However, we identified photosensitization as the underlying cause of KP dermal toxicity.