Two-photon fluorescence-guided precise photothermal therapy located in a single cancer cell utilizing bifunctional N-doped carbon quantum dots.

The utilization of carbon quantum dots (CQDs) for photothermal therapy has emerged as a hot research topic. However, there has been limited research on killing one single cancer cell which is critical in reducing unnecessary damage to the surrounding healthy tissues. In this work, we developed a two-photon fluorescence-guided precise photothermal therapy in a single human malignant melanoma (A375) cancer cell utilizing bifunctional N-doped CQDs. Resulting from the two-photon fluorescence of the CQDs, one single cancer cell can be located and simultaneously destroyed by the photothermal effect of the same CQDs. Specifically, the balanced two-photon absorption cross-section (7000 GM) and photoluminescence quantum yield (8.4%) of the CQDs enable the fluorescence-guided photothermal treatment to be achieved in only 5 s under the irradiation of 800 nm laser of 27.5 mW, much faster than the control experiment without the guidance of fluorescence. The heat generated by the aggregated CQDs is in sufficient amounts while being confined in a small area, as evidenced by the numerical simulations and photothermal experiments, to limit the range of thermal treatment in the cells. This work provides a new approach for realizing photothermal therapy with minimal damage and establishes a new application scenario of CQDs for precise tumor ablation.

Sixty-day repeated dose toxicity of sinafloxacin in rats and dogs.

Sinafloxacin is a new quinolone antibacterial agent. The present study was conducted to determine its toxicity at low flow rate intravenous infusion doses of 0, 10, 30, and 60 mg/kg/day in rats and at 0, 25, 50, and 100mg/kg/day in dogs 6 days per week for 60 days. A 20-day recovery period was included at the end of the study to evaluate the reversibility of the toxic effects. During the treatment and recovery periods, the effects of the test agent on mortality, body weight, food consumption, hematology, serum biochemistry, urinalysis, electrocardiogram (ECG), organ weights, bone marrow, and histopathology were examined. There were no treatment-related mortalities. Dysphoria and local irritation were observed in rats during administration, but the rats recovered soon after administration. Dysphoria, dermal rubeosis, salivation, vomiting and local irritation were observed in dogs receiving 50 or 100mg/kg/day during administration, but all dogs also recovered within 30 min after infusion. Significant increases in total bilirubin and glucose, and a significant decrease in total protein were observed in rats receiving the 60 mg/kg/day dose at the end of treatment period, but the levels returned toward normal during the 20-day recovery period. The most apparent toxicity was the digestive system of both rats and dogs, with irritation also occurring in the vein used for infusion. There were also notable effects on the endocrine system in rats and the central nervous system (CNS) in dogs. However, these toxic effects of sinafloxacin were transient and were reversible. The no-observed adverse effect level (NOAEL) in rats and dogs was 30 mg/kg/day and 25 mg/kg/day, respectively.

Protective effects of dehydrocavidine on carbon tetrachloride-induced acute hepatotoxicity in rats.

AIM OF THE STUDY: To investigate the protective effects of dehydrocavidine (DC), a main active ingredient of Corydalis saxicola Bunting (Yanhuanglian), on carbon tetrachloride (CCl4)-induced hepatotoxicity and the possible mechanisms involved in male Sprague-Dawley rats. MATERIALS AND METHODS: Acute hepatotoxicity was induced by CCl4 intoxication in rats. Serum biological analysis, lipid peroxides and antioxidants estimation, histopathological studies were carried out. RESULTS: Both pre-treatment with DC prior to CCl4 administration and post-treatment with DC after CCl4 administration significantly prevented increases in serum enzymatic activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and total bilirubin (TBIL). In addition, pre- and post-treatment with DC also significantly prevented formation of hepatic malondialdehyde (MDA), depletion of glutathione peroxidase (GPx) and depression of superoxide dismutase (SOD) in the liver of CCl4-intoxicated rats. ALT, AST, LDH, ALP and TBILL levels, as well as MDA, SOD and GPx activities were unaffected in normal rats by treatment with DC alone. GST, a phase II enzyme, had no significant changes during our experiments. Histopathological changes induced by CCl4 were also significantly attenuated by DC treatment in both preventive and curative experiments. CONCLUSIONS: DC has a potent hepatoprotective effect on CCl4-induced liver injury in rats through its antioxidant activity.