Phthalate induced toxicity in prostate cancer cell lines and effects of alpha lipoic acid.

OBJECTIVE: The effects of dimethyl phthalate, diethyl phthalate, diisobutyl phthalate, di-n-butyl phthalate, benzylbutyl phthalate, di-2-ethylhexyl phthalate were investigated on human prostate cancer cell lines DU145 and PC3 in vitro. MATERIALS AND METHODS: Standards of dimethyl phthalate, diethyl phthalate, di-isobutyl phthalate, dibutyl phthalate, benzyl butyl phthalate, and di-ethyl hexyl phthalate were used. Alpha lipoic acid was used as antioxidant compound. DU145 and PC3 human prostate carcinoma cells were used. MTT assay were used for cytotoxicity assay. RESULTS: A low dose proliferative effect of phthalates in vitro was observed. With the hypothesis of the inhibition of aerobic glycolysis activity in cancer treatment, α-lipoic acid was applied to cells; where as a contrary to previous studies, no change in the cell proliferation was observed. In combination with ALA, at IC50 and lower doses, an increase of the cytotoxic effect was found for DIBP, DBP and BBP; while for DMP, DEP and DEHP, a decrease was observed for DU145 cells. In PC3 cells, a decrease was observed for DMP, DEP and DBPs; while no significant difference were observed for DEHP, DIBP and BBP. CONCLUSSION: The present study demonstrates preliminary information regarding the low dose proliferative effects of phthalates in prostate cancer in vitro (Tab. 2, Fig. 2, Ref. 65).

Antioxidant therapy impresses in oxidative stress-induced kidney cells.

INTRODUCTION:   Renal cell cancer (RCC) is not a single entity, but consists of different types of tumors derived from various parts of the nephron (epithelium or renal tubules). It is known that cancer initiation and progression is related to the balance between oxidants and antioxidants directly. Interestingly, advanced stages of cancer such as metastasis, angiogenesis are associated with cell oxidative capacity. Familiar antioxidative substances such as carotenes and vitamin C inhibit oxidation of other molecules during carcinogenesis. They can define the distinction between cancer and normal cells, destroying cancer cells while stabilizing healthy cells. METHODS:   apoptotic activities of kidney cells were measured with caspase Elisa kits. DNA laddering test was used to show DNA damage in H2O2 condition. RESULTS:   For tumor mechanism, they act as pro-oxidants, producing hydrogen peroxide that attacks the cancer, whereas, in normal conditions they act as protective antioxidants. CONCLUSIONS:   The unlike reaction of specific antioxidants should be known at different cell stages. The aim of this study was to assess the antioxidative roles of alpha lipoic acid on kidney cancers during oxidative stress induction (Tab. 1, Fig. 7, Ref. 27).

GSM-like radiofrequency exposure induces apoptosis via caspase-dependent pathway in infant rabbits.

BACKGROUND: There have been several Radio Frequency (RF) field researches on various populations and groups of different ages in recent years. However, the most important group for research has been declared as the pregnant women and their babies. OBJECTIVE: The aim of the study was to analyse the effect on apoptotic factors of RF fields on newborn rabbit liver tissues. MATERIALS AND METHODS: Cytochrome c and AIF (Apoptosis Inducing Factor) levels were measured by western blot and caspase 1, 3 and 9 activities were measured by colorimetric method. RESULTS: Cytochrome c and AIF levels were not altered, but all caspase activities were increased in female infant rabbits that exposed to 1800 MHz GSM-like RF signals when they reached 1 month of age and caspase 1 and caspase 3 levels were decreased in male infant rabbits that exposed to 1800 MHz GSM-like RF signals between 15th and 22nd days of the gestational period. Results showed that 1800 MHz GSM-like RF exposure might lead to apoptosis in infant rabbit's liver tissues. CONCLUSION: According to the results, we suggest that postnatal RF exposure causes caspase dependent apoptosis in female infant rabbits liver tissues (Tab. 1, Fig. 2, Ref. 27).

The cell death pathway induced by metal halide complexes of pyridine and derivative ligands in hepatocellular carcinoma cells - necrosis or apoptosis?

BACKGROUND: Drugs designed to restore programmed cell death might be effective against many cancer. It was aimed to study the possible apoptotic-necrotic effects of the pyridinehalide complexes such as dichlorodipyridinepalla-dium(ll) (PdCl2L1(2)), dichlorodipyridinenickel(ll) (NiCl2L1(2)), dichlorodipyridinecopper(ll) (CuCl2L1(2)), dibromodipyridinecopper(ll) (CuBr2L1(2)) and dichlorobis-(2,4-dimethylpyridine)copper(ll) (CuCl2L2(2)) in the hepatocarcinoma cells (Hep G2). METHODS: All complexes were characterized by elemental analysis, 1H-NMR, FT-IR and Far-IR spectroscopy. Apoptotic effects were evaluated by cell viability assay, DNA laddering assay, LDH assay, DAPI nuclear staining and caspase 1-3-9 activity analysis. RESULTS: According to cell proliferation/viability datas, CuCl2L2(2) was estimated the most toxic, NiCl2L1(2) the least toxic complex. Treatment of CuCl2L2(2) in IC50 doses resulted in a remarkable increase lactate dehydrogenase, it was followed by CuBr2L1(2) complex. Picnotic nuclei, anisonucleosis and nuclear condensations in 200 microM concentration of CuCl2L2(2) and CuCl2L1(2) treated cells were observed with DAPI staining also DNA brakes were also determined with electrophoresis. Caspase 1,3 and 9 increased activation were not detected. CONCLUSIONS: The present study results indicate that, PdCl2L1(2), NiCl2L1(2), CuCl2L1(2), CuBr2L1(2), CuC12L2(2) complexes have antiproliferative action on hepatocellular carcinoma cells. However it would be wrong to interpret this effect as an apoptosis or necrosis exactly.

Serum neopterin, sialic acid and nitric oxide levels in dogs with malignant mammary tumours.

Mammary cancer is one of the leading causes of death in pet population. Early diagnosis and malignancy detection is important for prognosis. The levels of neopterin, sialic acid and nitric oxide in serum of dogs with malignant mammary tumours were evaluated to investigate the importance of these biochemical parameters for malign mammary tumour. Twelve healthy dogs and twenty dogs with malignant mammary tumours were used as research materials. Blood samples were collected from both groups for neopterin analysis by enzyme-linked immunosorbent assay, whereas nitric oxide and sialic acid were measured by modified nitrate reductase method and spectrophotometry, respectively. Tissue specimens were evaluated and defined as malignant tumours. Serum nitric oxide and sialic acid levels in dogs with mammary tumours were significantly higher than those in the healthy dogs. Serum neopterin levels were not found significantly different in dogs with mammary tumours compared to healthy dogs. Malignancy of canine mammary tumours are accompained by an elevation of nitric oxide and sialic acid levels.