Does Boric Acid Inhibit Cell Proliferation on MCF-7 and MDA-MB-231 Cells in Monolayer and Spheroid Cultures by Using Apoptosis Pathways?

Most breast cancers originate in the lobules or ducts of the breast. Breast cancer as the second main cause of death among women in the world is the most common kind of cancer in women. Studies have been conducted to find the optimal treatment for breast cancer. Moreover, the therapeutic effects of different drugs and substances on this disease have been intensively researched. Boric acid accounts for 96% of the boron content in body fluids, and its derivatives are absorbed by the human body. It is assumed to be represented as (B(OH)2). Experimental studies have shown a reduction of cell proliferation and stimulation of apoptosis in some melanoma, prostate, and colon cancer cell lines through boric acid. The aim of this study was to investigate if boric acid could be used for treating breast cancer. The impacts of boric acid on the human breast carcinoma cell lines MCF-7 and MDA-MB-231 were studied with TUNEL, BrdU, caspase-3, and endo-G immunohistochemical studies in 3D and 2D culture systems. Furthermore, we conducted a qRT-PCR study to show changes in the expression of some genes involved in apoptosis. Suppression of cell proliferation through boric acid-inducing apoptosis was observed both in 3D and 2D culture conditions. These results are compatible with the gene expression results. The ENDOG, CASP3, CASP8, and CASP9 gene expression significantly changed at all time intervals in MCF-7 and MD-MB-231 cell lines boric acid can potentially treat breast cancer as an anti-cancer agent candidate.

Histochemical, Immunohistochemical, and Biochemical Investigation of the Effect of Resveratrol on Testicular Damage Caused by Methotrexate (MTX).

Cancer is one of the world's major causes of death. The aim of this study is to examine the acute effects of resveratrol on testicular toxicity, oxidative stress, and apoptosis caused by MTX, which is widely used in the treatment of many diseases, especially cancer, histochemically, immunohistochemically, and biochemical methods using different parameters. A total of 32 Wistar albino male rats were randomly divided into 4 groups: control, resveratrol (RES), MTX, and MTX + RES, with 8 animals in each group. At the end of the experiment, tissue and blood samples were taken, and histochemical, immunohistochemical, and biochemical parameters were examined. In this study, where parameters were compared for the first time, total thiol (TT) and native thiol (NT) are the highest in the RES group, disulfide (DS), and ischemia-modified albumin (IMA) are the highest in the MTX group. Total oxidant status (TOS) and oxidative stress index (OSI) are the highest in the MTX group, and total antioxidant status (TAS) is the highest in the RES group. Separation and deterioration in the tunica albuginea, congestion and edema in the interstitial region, vacuolization in the seminiferous epithelium, and spermatogenic serial cells spilling into the lumen without completing their maturation were observed. When examined in terms of histochemical, immunohistochemical, and biochemical examinations, our study revealed that resveratrol has positive effects on methotrexate-induced acute testicular damage, oxidative stress, and apoptosis.

Irisin: a potentially candidate marker for myocardial infarction.

Myocardial infarction (MI) causes energy depletion through imbalance between coronary blood supply and myocardial demand. Irisin produced by the heart reduces ATP production by increasing heat generation. Energy depletion affects irisin concentration in circulation and cardiac tissues, suggesting an association with MI. We examined: (1) irisin expression immunohistochemically in rat heart, skeletal muscle, kidney and liver in isoproterenol (ISO)-induced MI, and (2) serum irisin concentration by ELISA. Rats were randomly allocated into 6 groups (n=6), (i) control, (ii) ISO (1h), (iii) ISO (2h), (iv) ISO (4h), (v) ISO (6h), and (vi) ISO (24h), 200mg ISO in each case. Rats were decapitated and the blood and tissues collected for irisin analysis. Blood was centrifuged at 1792 g for 5 min. Tissues were washed with saline and fixed in 10% formalin for histology. Serum irisin levels gradually decreased from 1h to 24h in MI rats compared with controls, the minimum being at 2h, increasing again after 6h. Cardiac muscle cells, glomerular, peritubular renal cortical interstitial cells, hepatocytes and liver sinusoidal cells and perimysium, endomysium and nucleoi of skeletal muscle were irisin positive, but its synthesis decreased 1-4h after MI. At all time-points, irisin increased near myocardial connective tissue, with production in skeletal muscle, liver and kidney recovering after 6h, although slower than controls. Unique insight into the pathogenesis of MI is shown, and the gradually decrease of serum irisin might be a diagnostic marker for MI.