In the last two decades, fluorescent carbon quantum dots (CQDs) have attracted intense interest as a new fluorescent nanomaterial with unique properties. This material offers significant advantages compared with conventional dyes and inorganic QD systems, and is used extensively in many different fields, especially in bioimaging and sensor applications. Despite all the positive values they offer, the production of CQD systems with excitation wavelength-dependent nature and high quantum yield (QY) is still a scientific challenge. In this study, we proposed the fabrication of CQD through a facile and easy-to-tune hydrothermal method using cheap and biocompatible precursors such as urea and lactic acid. The effect of experimental parameters including synthesis time, temperature, and mass ratio of the precursors, were determined to obtain the highest QY (48%). The as-prepared nitrogen-doped (N-doped) CQDs exhibited robust stability in the dark and in a wide range of pH values with excitation wavelength-dependent properties. Additionally, CQDs showed remarkable sensitivity and selectivity in the sensing of Fe3+ in blood plasma with a linear correlation in the range of 0–1000 μM, indicating the high potential of CQDs in practical applications. Lastly, cytotoxicity and antibacterial activity tests demonstrated the low toxicity and high biocompatibility of proposed CQDs. Considering the facile and efficient synthetic method, easy-to-tune optical properties, excitation-dependent nature, high fluorescence activity, and low cytotoxicity, we strongly anticipate that N-doped CQDs could provide unique advantages in various biomedical applications including diagnosis, bioimaging, and biosensors.

Butylated hydroxyanisole (BHA) has been widely used in the cosmetics, pharmaceutical, and food industries due to its antioxidant activity. Despite the antioxidant effects, reported adverse effects of BHA at the cellular level have made its use controversial. In this regard, this study was performed to elucidate the potential toxicity mechanism caused by BHA at the molecular level in zebrafish embryos. For this purpose, zebrafish embryos were exposed to BHA at levels of 0.5, 1, 5, 7.5 and 10 ppm and monitored at 24, 48, 72 and 96 hours. Survival rate, hatching rate and malformations were evaluated. We examined the potential for reactive oxygen species (ROS) production and apoptosis signalling accumulation in the whole body. Moreover, we evaluated histopathological and immunohistochemical (8-OHDG) characterization of the brain in zebrafish embryos at the 96th hour. We also examined apoptosis, histopathological and immunohistochemical (8-OHDG) characteristics in 96 hpf zebrafish larvae exposed to tertiary butylhydroquinone (TBHQ), one of the major metabolites of BHA, at doses of 0.5, 2.5, 3.75 and 5 ppm. Consequently, it has been considered that increased embryonic and larval malformations in this study may have been caused by ROS-induced apoptosis. After 96 h of exposure, positive 8-OHdG immunofluorescence, degenerative changes, and necrosis were observed in the brain of BHA and TBHQ-treated zebrafish larvae in a dose-dependent manner. BHA and TBHQ exposure could lead to an increase in 8-OHdG activities by resulting oxidative DNA damage. In particular, the obtained data indicate that the induction of ROS formation, occurring during exposure to BHA and/or multiple hydroxyl groups, could be responsible for apoptosis.

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