Ionized alkaline water reduces injury in BALB/c mice infected with Leishmania amazonensis.

Ionized water has been reported to contribute to the tissue repair process and wound healing. Water purifiers can generate ionized water by means of activated charcoal with silver and minerals, the main purpose of which are to reduce microbiological and physicochemical contaminants. Moreover, when water is subjected to a magnetic field an organization of water molecules occurs due to the presence of mineral salts. The resulting water is thus more alkaline, which has been shown to be non-toxic to mice and can actually prolong survival. Cutaneous leishmaniasis is a neglected tropical disease, caused by obligate uni- and intracellular protozoa belonging to the genus Leishmania, that can manifest in the form of skin lesions. Thus, the objective of this study was to compare the evolution of disease in L. amazonensis-infected BALB/c mice that received tap water (TW) or ionized alkaline water (IAW). As a control, additional groups of mice receiving TW or IAW were also treated with the antileishmanial miltefosine. All mouse groups received either TW or IAW as drinking water 30 days prior to infection and the groups continued to receive the respective drinking water for 4 weeks, after which the blood and plasma were collected. Biochemical assays of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase, creatinine, urea, glucose, triglycerides, and cholesterol were performed, in addition to hematology tests. There was a significant decrease in the volume of the lesion for groups that received IAW, in which the ingestion of ionized alkaline water favored the non-evolution of the lesion in the footpads of the animals. The results of the blood count and leukogram tests were within the normal values for BALB/c mice demonstrating that ionized water has no toxic effects on blood factors.

ß-Carboline-α-aminophosphonate Derivative: A Promising Antitumor Agent for Breast Cancer Treatment.

Breast cancer is the most common type of cancer and the leading cause of cancer mortality among women worldwide. Considering the limitations of the current treatments available, we analyzed the in vitro cytotoxic potential of ((4-Fluoro-phenyl)-{2-[(1-phenyl-9H-ß-carboline-3-carbonyl)-amino]-ethylamino}-methyl)-phosphonic acid dibutyl ester (BCP-1) in breast cancer cells (MCF-7 and MDA-MB-231) and in a non-tumor breast cell line (MCF-10A). BCP-1 has an α-aminophosphonate unit linked to the ß-carboline nucleus, and the literature indicates that compounds of these classes have high biological potential. In the present study, the mechanism of action of BCP-1 was investigated through methods of spectrofluorimetry, flow cytometry, and protein expression analysis. It was found that BCP-1 inhibited the proliferation of both cancer cell lines. Furthermore, it induced oxidative stress and cell cycle arrest in G2/M. Upregulation of apoptosis-related proteins such as Bax, cytochrome C, and caspases, as well as a decrease in the anti-apoptotic protein Bcl-2, indicated potential induction of apoptosis in the MDA-MB-231 cells. While in MCF-7 cells, BCP-1 activated the autophagic death pathway, which was demonstrated by an increase in autophagic vacuoles and acidic organelles, in addition to increased expression of LC3I/LC3II and reduced SQSTM1/p62 expression. Further, BCP-1 demonstrated antimetastatic potential by reducing MMP-9 expression and cell migration in both breast cancer cell lines. In conclusion, BCP-1 is a promising candidate for breast cancer chemotherapy.

Dibenzylideneacetone Induces Apoptosis in Cervical Cancer Cells through Ros-Mediated Mitochondrial Damage.

Cervical cancer is a health problem among women worldwide. Considering the limitations of prevention and antineoplastic chemotherapy against cervical cancer, research is needed to discover new, more effective, and safe antitumor agents. In the present study, we investigated the in vitro cytotoxicity of a new synthetic dibenzylideneacetone derived from 1,5-diaryl-3-oxo-1,4-pentadienyl (A3K2A3) against cervical cancer cells immortalized by HPV 16 (SiHa), and 18 (HeLa) by MTT assay. Furthermore, we performed spectrofluorimetry, flow cytometry, and Western blot analyzes to explore the inhibitory mechanism of A3K2A3 in cervical cancer cells. A3K2A3 showed cytotoxic activity against both cell lines. Mitochondrial depolarization and reduction in intracellular ATP levels were observed, which may be dependent on the redox imbalance between increased ROS and reduced levels of the antioxidant defense. In addition, damage to the cell membrane and DNA, and effective blocking of cell division in the G2/M phase were detected, which possibly led to the induction of apoptosis. This result was further confirmed by the upregulation of apoptosis-related proteins Bax, cytochrome C, and caspases 9 and 3. Our results provided the first evidence that A3K2A3 contributes to the suppression of cervical cancer in vitro, showing promise as a possible alternative for the treatment of this cancer.