Rationale and technique of malaria control
David A Warrell, Herbert M Gilles in Essential Malariology, 2017
Later, a number of synthetic repellents were developed, with a duration of protection of 2–4 hours. The most useful of these are indalone, Rutgers 612, dimethyl phthalate (DMP), dibutyl phthalate (DBP) and a mixture known as 6–2–2. The most effective against Anopheles is DBP (average protection 4 hours) and DMP (average protection 3 hours). Several newer compounds are now available and among these N,N-diethyl-3-methylbenzamide (DEET) appears to be the best repellent against many blood-sucking arthropods. It can be active for as long as 10 hours. It is frequently used in the form of a 50 per cent solution in alcohol, but is available in a wide range of concentrations and formulations such as lotions, creams, gels, aerosols, pump sprays and towlettes. It is a major ingredient in 90 per cent of commercial repellents.
Effects of chemical exposures on testis cell-cell interactions and endocrine function
C. Yan Cheng in Spermatogenesis, 2018
Chemicals may block AR binding and activation by endogenous androgen. For example, the fungicide vinclozolin has been shown to bind DNA and inhibit dihydrotestosterone- (DHT-) induced transcriptional activation of the AR.29 Similarly, the phthalate esters dibutyl phthalate (DBP) and di(2-ethylhexyl) phthalate (DEHP) inhibited AR transcriptional activity and disrupted sexual differentiation in male rats.30,31 DDT-related compounds inhibited hepatic mono-oxygenase activity, thereby promoting androgen degradation and disruption of AR-mediated activity.32 Interestingly, BPA decreased E2 secretion while DEHP increased aromatase expression and E2 biosynthesis in rodent testis, which increased serum E2 concentrations (Figure 19.2).33,34 Therefore, the estrogenic and/or antiandrogenic activity of EDCs possibly varies with the tissue and stage of development, and dosage and duration of chemical exposure.
Hazard Characterization and Dose–Response Assessment
Ted W. Simon in Environmental Risk Assessment, 2019
The difficulty in determining adversity can be illustrated by EPA’s IRIS database entry for the pesticide oxadiazon (https://cfpub.epa.gov/ncea/iris/iris_documents/documents/subst/0253_summary.pdf#nameddest=rfd). Rats were administered diets containing 0, 10, 100, 1000, or 3000 parts per million (ppm) oxadiazon. At a dietary concentration of 100 ppm, increased levels of serum proteins in 18% of females and increased liver weights in 31% of both sexes were observed, and these were chosen as the critical effect. The NOAEL was 10 ppm and the LOAEL was 100 ppm. At 1000 ppm, hepatotoxicity, hemolytic anemia, and kidney effects were observed. Were the serum protein changes and increase in liver weights in the minority of animals tested truly an adverse effect? Perhaps these represented an adaptive or compensatory response within the biological capacity of the animals. Certainly, hepatotoxicity and anemia are adverse. Perhaps these higher-dose effects would be more appropriately chosen as adverse rather than adaptive effects. Compare these effects with the critical effect of mortality chosen for dibutyl phthalate (https://cfpub.epa.gov/ncea/iris/iris_documents/documents/subst/0038_summary.pdf#nameddest=rfd). Which effect do you think is truly adverse?
Effect of substitution of plasticizer dibutyl phthalate with dibutyl sebacate on Eudragit® RS30D drug release rate control
Published in Pharmaceutical Development and Technology, 2019
Rakesh Singh Chaudhary, Tejas Patel, Job Richard Kumar, Mohamed Chan
The objective of this study was to evaluate an alternative plasticizer for the film coating formulation containing Eudragit® RS polymer dispersion for the drug release coating system for diltiazem hydrochloride controlled release pellets. The effect of substitution of dibutyl phthalate with alternative plasticizer dibutyl sebacate in the same amount will be evaluated to establish that there is no change in the drug release profile for the coated controlled release pellets. The alternative plasticizer dibutyl sebacate for Eudragit® RS 30D polymer is selected as it lowers the glass transition temperature of the polymer during the coating process to similar extent as dibutyl phthalate and improves the mechanical strength of the coating (Zelkó et al. 2002; Saeltone et al. 1995). The use of dibutyl sebacate as plasticizer for the brittle polymers is recommended in the range of 5–30% (Nollenberger and Albers 2013). The of dibutyl sebacate as plasticizer for Eudragit® RS 30D polymer is related to its effectiveness and influence on the permeability on the film formed. The recommended amount of dibutyl sebacate for Eudragit® RS 30D is up to 20% of the dry polymer content (Rowe et al. 1984). The study is designed to identify a suitable replacement of dibutyl phthalate with another plasticizer with similar physical and chemical properties without impacting the performance of the finished product.
Fabrication of solid lipid nanoparticles-based patches of paroxetine and their ex-vivo permeation behaviour
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Fahad Pervaiz, Ayesha Saba, Haya Yasin, Manal Buabeid, Sobia Noreen, Abida Kalsoom Khan, Ghulam Murtaza
Dibutyl-phthalate was used as a plasticizer, as it helps to soften the polymer matrix by diffusing it. It reduces the interactions between the polymer molecules like hydrogen bonding and also forms a bond with polymer molecules that helps in the film formation [23]. The effect of particle size on permeation was also analysed. The results showed that permeation increases with decreased particle size, i.e. the smaller the particle size, the higher the surface of particles, and more intimate their contact with corneocytes, thus a greater the penetration of the drug through stratum corneum [36]. When the effect of surfactant on permeation was analysed, it was observed that there was an increase in permeation of drug through the skin with an increase in surfactant to lipid ratio. Likely, the surfactant helps to loosen the lipid bilayers of the stratum corneum, thus enhancing drug penetration. Similar observations were explained in other studies [51].
Testicular developmental impairment caused by flutamide-induced and DEHP-induced cryptorchid rat models is mediated by excessive apoptosis and deficient autophagy
Published in Toxicology Mechanisms and Methods, 2018
Yi Wei, Yu Zhou, Xiang-Liang Tang, Bin Liu, Lian-Ju Shen, Chun-lan Long, Tao Lin, Da-wei He, Sheng-de Wu, Guang-hui Wei
Mylchreest et al. (Mylchreest et al. 1999) compared the effects of dibutyl phthalate (DBP) and the antiandrogen flutamide using a shorter exposure during the prenatal period of male sexual differentiation in rats. They demonstrated that Flu and DBP disrupted the androgen signaling necessary for male sexual differentiation but with a different pattern of antiandrogenic effects. Similarly, Vo et al. (Vo et al. 2009) compared differential effects of flutamide and DEHP on male reproductive organs. In their study, serum testosterone was upregulated by Flu and it was down-regulated by DEHP. In addition, they found differential gene expression patterns by microarray analysis following ED exposure. Although Flu and DEHP are considered to be identical with regard to their anti-androgenic effects, their effects on developing male reproductive organs were distinct. Therefore, whether autophagy and apoptosis process participates in the regulation of testicular impairment in cryptorchidism testis is largely unknown and if DEHP-induced and Flu-induced cryptorchid rats led to reproductive injury with a different pattern of autophagic effects is also unclear.
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