The rapid synthesis techniques and interesting multidisciplinary applications make carbon nanodots (CNDs) stand out from semiconductor quantum dots. Moreover, CNDs derived from green precursors have gained more importance beyond chemically derived CNDs due to sustainable synthesis opportunities. However, the presence of molecular impurities or intermediates or fluorophores was neglected during the entire process. Herein, we illustrate the sustainable synthesis of CNDs from Hemigraphis alternata plant leaves with extended carbonization procedure (3 and 9 min) along with simultaneous ethylene glycol and diethyl ether solvent treatment method for the successful removal of interfering fluorophores. To unravel the distinction between purified CNDs (P-CNDs) and organic fluorescent carbon nanostructures (org-FCNs), we carried out photophysical, structural, and morphological studies. A quantum yield (QY) of 69 and 42% was observed for crude org-FCNs, and crude P-CNDs; however after purification, QY of 1% and absence of one component from the fluorescent decays curve suggest the removal of fluorophores. Further, HR-TEM and DLS studies showed the quasi-spherical amorphous particles having < 10 nm particle size for P-CNDs. Besides, in vitro biocompatibility investigation and cellular uptake assay (1–100 μg/mL) against the MDA-MB 468 cell lines proves the ≥ 95% cell viability and good internalization for both org-FCNs and P-CNDs. Hence, our study shows the presence of fluorophore impurities in plant-derived CNDs, the removal and resemblance in biocompatibility properties. Hence, this information can be considered during the synthesis and isolation of CNDs. Simple and effective removal of impurities to harvest pure carbon nanodots (CNDs) through solvent-based selective separation method, and revelation of the cocktail flourphores similar to biocompatible blue fluorescent CNDs were studied.

In this study, we report a controlled one-pot green synthesis of multiwalled carbon nanotubes (MWCNTs) via pyrolysis of sustainable agriculture waste (chickpea peel) at 400 °C in aqueous medium. These MWCNTs demonstrated 7.0 nm diameter, 0.28 nm graphitic spacing with carbonyl, hydroxyl, and carboxylic acid functionality. The D band (presence of sp3 defects) and G band ( E2g mode of graphite) at 1350 cm−1 and 1580 cm−1 originated in Raman spectrum, respectively. The prepared MWCNTs showed blue fluorescence with 10% fluorescence quantum yield in aqueous medium. The MWCNTs showed triple exponential decay characteristics with an average fluorescence lifetime of 4.7 ns. The synthesized MWCNTs revealed a consistent fluorescence in the cytoplasm of 22RV1 human prostate carcinoma cell line without exerting any sign of cytotoxicity. The MWCNTs also exhibited remarkable cytocompatibility in human immortalized prostate epithelial RWPE1 cells.

The purpose of this study was to examine the characteristics of acetaminophen (APAP)-induced liver damage, using fluorescence bioimaging, serum biochemistry, and histopathology. At six weeks of age, eighteen mice were divided into three groups as group 1 (G1) as control, group 2 (G2) as fluorescence probe control and group 3 (G3) as APAP-treated. G3 mice were orally treated with APAP (800 mg/kg b.w.), while G1 and G2 mice were treated with 0.9% saline. Twenty-two hours after APAP treatment, G2 and G3 mice were intravenously treated with Annexin-Vivo 750 as probe, while G1 mice were treated with saline. Fluorescence bioimaging was performed at two hours after probe treatment. The mice were sacrificed and serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and lactate dehydrogenase were analyzed. Liver damage was examined by hematoxylin and eosin (H&E) staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. In vivo bioimaging, fluorescence intensity of the region of interest (ROI) was significantly increased in the livers of G2 and G3 mice compared with those in G1 mice (p<0.05 and p<0.01). In addition, ex vivo bioimaging confirmed that the fluorescence intensity of the ROI was significantly increased in the livers of G2 and G3 mice compared with those in G1 mice (p<0.05 and p<0.01). All examined serum parameters of G3 were significantly increased compared with G1 and G2 (p<0.05 and p<0.01). H&E examination showed acute hepatic cell necrosis in the livers of G3 mice, while there was no cell death in the livers of G1 and G2 mice. TUNEL staining also showed many cell death features in G3 mice, whereas no pathological findings were shown in G1 or G2 mice. In summary, fluorescence bioimaging showed the possibility of cell death detection in the livers of mice treated with APAP, and this was corroborated by serum chemistry and histopathological examination.

The purpose of this study was to investigate the lesions of a mouse collagen antibody-induced arthritis (CAIA) model using fluorescence bioimaging and micro-computed tomography (micro-CT) and to compare it with histopathological examination. Twelve mice were randomly divided into three groups: group 1 (G1) as control, group 2 (G2) as fluorescence probe control and group 3 (G3) as collagen antibodyinduced arthritis. The mice of G3 intravenously received anti-type II collagen 5-clone antibody cocktail (2 mg/mouse) on day 0 and intraperitoneally received lipopolysaccharide (50 μg/mouse) on day 3. On the while, the mice of G1 and G2 received 0.9% saline in equal volumes at equivalent times. Fluorescence bioimaging and micro-CT analysis were carried out to assess arthritis. Treatment with the collagen antibody cocktail increased the paw thickness of mice compared to those in both the control and probe-treated groups. Fluorescence bioimaging using a near infrared imaging agent showed high intensity in the joints of collagen antibody- treated mice, whereas those of control mice showed no signal. Micro-CT analysis of the knee joints of collagen antibody-treated mice showed rough and irregular articular appearance, whereas those of control mice showed normal appearance. Histopathological examination of the knee joints of collagen antibody-treated mice revealed destruction of cartilage and bony structure, synovial hyperplasia and infiltration of inflammatory cells. No cartilage destruction or inflammation was observed in control or probe control mice. Taken together, it is concluded that analyses of fluorescent bioimaging made it possible to evaluate CAIA lesions, comparable with those by micro-CT and histopathological examination in mice.