Carlos Alberto de Souza Costa

Ellagic acid derivatives, ellagitannins, proanthocyanidins and other phenolics, vitamin C and antioxidant capacity of two powder products from camu-camu fruit (Myrciaria dubia)

The aims of this study were the evaluation of polyphenols and vitamin C content, and antioxidant capacity of dehydrated pulp powder and the dried flour obtained from the skin and seeds residue remaining after pulp preparation from camu-camu (Myrciaria dudia). Fifty-three different phenolics were characterised by HPLC-DAD-ESI-MS-MS and UPLC-HR-QTOF-MS-MS. The phenolic content of camu-camu flour was higher than that of the pulp powder (4007.95 mg/100 g vs. 48.54 mg/100 g). In both products the flavonol myricetin and conjugates, ellagic acid and conjugates and ellagitannins were detected. Cyanidin 3-glucoside, and quercetin and its glycosides were only found in the pulp powder, while proanthocyanidins were only present in the flour (3.5 g/100 g, mean degree of polymerisation 3). The vitamin C content was lower in pulp powder (3.5%) than in the flour (9.1%). The radical-scavenging capacity of both powders was determined by the DPPH, ABTS and ORAC assays, and was higher for camu-camu flour as could be expected for its higher phenolics and vitamin C content. Comparative analyses with fresh camu-camu berries indicate that some transformations occur during processing. Analysis of fresh berries showed that ellagic acid derivatives and ellagitannins were mainly present in the seeds, while proanthocyanidins were present both in the seeds and skin.

Photodynamic Therapy to Eradicate Tumor Cells

The cell cycle is a collection of highly ordered processes involving numerous regulatory proteins that guide the cell through a specific sequence of events culminating in the duplication of the cell (Elledge, 1996). In general, the cell cycle can be altered to the advantage of many factors. Three basic cell cycle defects are mediated by misregulations of cyclin-dependent kinases (CDKs), unscheduled proliferation, genomic instability (GIN) and chromosomal instability (CIN). In the first case, mutations result in constitutive mitogenic signaling and defective responses to anti-mitogenic signals. The second, GIN, leads to additional mutations (Kastan & Bartek, 2004), and CIN is responsible for numerical changes in chromosomes (Lee et al., 1999). Moreover, data suggest that the mutations leading to tumorigenesis are even more numerous and heterogeneous than previously thought (Hudson et al., 2010). This accumulation of genetic mutations can arise by nucleotide substitutions, small insertions and deletions, chromosomal rearrangements and copy number changes that can affect protein-coding or regulatory components of genes. Cancer genomes usually acquire somatic epigenetic “marks” compared to non-neoplastic tissues from same organ (Hudson et al., 2010). In this context, a neoplasm (Greek, neo = new + plasis = growth) can be defined as an abnormal mass of tissue whose growth exceeds and is uncoordinated with that of the normal tissue, and persists in the same excessive manner after cessation of the stimuli that initiated the change.