Evaluation of the Toxic Effects of Aluminum Hydroxide Nanoparticles as Adjuvants in Vaccinated Neonatal Mice.

Aluminum hydroxide nanoparticles have been employed in many industries, which are widely abundant in many aspects of human life. The role of the aluminum hydroxide nanoparticles adjuvant is to enhance the immune response. However, the impact of nanoparticles exposure has not been perfectly investigated yet. Accordingly, some questions have been raised about their potentially harmful effects, based on which the current research aims to answer them. This study aimed to investigate the histological effects of aluminum hydroxide nanoparticles and bulk-aluminum hydroxide (bulk Al[OH]3) on the liver, lung, heart, and kidney tissues. For this reason, an experiment was implemented on the aluminum hydroxide nanoparticles adjuvant in five neonatal mice. Intramuscularly, the mice were injected with 0.125 mL of adjuvanted vaccine, while five neonatal mice were injected with bulk and nanoparticles of Al (OH)3 and then sacrificed after one and two months, respectively. Vaccines were controlled by evaluating the histopathological response in neonatal mice. Subsequently, the pathological effect of both adjuvants was surveyed using the histological study of the lung, liver, heart, and kidney of the animals. The obtained recorded data indicated that both types of vaccine adjuvants caused pathological lesions on the histology sections of the liver, lung, heart, and kidney tissues. Moreover, bulk Al (OH)3 adjuvant vaccine was more effective and had a higher pathological response than aluminum hydroxide nanoparticles adjuvant vaccine. In addition, the total DNA content in both groups was estimated using Fluorometer from Promega. Compared to aluminum hydroxide nanoparticles groups, the tissues indicated a decrease in total DNA content obtained in bulk Al (OH)3 groups. Therefore, it can be concluded that the exposure to aluminum hydroxide nanoparticles would result in less pronounced toxicity, as well as systemic inflammation, compared to the bulk Al (OH)3 aluminum hydroxide.

Artificial Light at Night of Different Spectral Compositions Differentially Affects Tumor Growth in Mice: Interaction With Melatonin and Epigenetic Pathways.

Lighting technology is rapidly advancing toward shorter wavelength illuminations that offer energy-efficient properties. Along with this advantage, the increased use of such illuminations also poses some health challenges, particularly breast cancer progression. Here, we evaluated the effects of artificial light at night (ALAN) of 4 different spectral compositions (500-595 nm) at 350 Lux on melatonin suppression by measuring its urine metabolite 6-sulfatoxymelatonin, global DNA methylation, tumor growth, metastases formation, and urinary corticosterone levels in 4T1 breast cancer cell-inoculated female BALB/c mice. The results revealed an inverse dose-dependent relationship between wavelength and melatonin suppression. Short wavelength increased tumor growth, promoted lung metastases formation, and advanced DNA hypomethylation, while long wavelength lessened these effects. Melatonin treatment counteracted these effects and resulted in reduced cancer burden. The wavelength suppression threshold for melatonin-induced tumor growth was 500 nm. These results suggest that short wavelength increases cancer burden by inducing aberrant DNA methylation mediated by the suppression of melatonin. Additionally, melatonin suppression and global DNA methylation are suggested as promising biomarkers for early diagnosis and therapy of breast cancer. Finally, ALAN may manifest other physiological responses such as stress responses that may challenge the survival fitness of the animal under natural environments.

Failure of pupillary dilation in early choroidal detachment.

Transient miosis presents a challenge in extracapsular cataract extraction and retinal detachment surgery, despite the advent of the small-pupil ophthalmoscope. Mechanisms have been proposed and preventive measures described. We describe a case of transient miosis that led to cancellation of the repair of retinal detachment and was the first sign of early choroidal detachment.