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Biomedical subjects

S M Piperakis

Publications and source records attributed to S M Piperakis.

15 recordsLinked to original sources
PubMed2006

Effects of pulsed electric fields on DNA of human lymphocytes.

The effects of pulsed electric fields of low frequency (50 Hz) on DNA of human lymphocytes were investigated. The influence of additional external factors, such as hydrogen peroxide (H2O2) and gamma-irradiation, as well as the repair efficiency in these lymphocytes, was also evaluated. The comet assay, a very sensitive and rapid method for detecting DNA damage at the single cells level was the method used. A significant amount of damage was observed after exposure to the electric fields, compared to the controls. After 2 h incubation at 37 degrees C, a proportion of damage was repaired. H2O2 and gamma-irradiation increased the damage to lymphocytes exposed to pulsed electric fields according to the dose used, while the amount of the repair was proportional to the damage.

Adult↗
PubMed2006

Measuring the effects of pesticides on occupationally exposed humans with the comet assay.

In this study we examine the effects of a mixture of pesticides on occupationally exposed agricultural workers. The study was performed on 149 people, 84 agricultural workers and 65 healthy men from the same area, who served as the control group. The exposed group was divided into a subgroup with 65 individuals moderately exposed (39 men and 26 women) and a highly exposed subgroup consisted of 19 men. The statistical analysis of the comet assay results showed that there were no significant differences in basal DNA damage between pesticide-exposed workers and the control group nor between moderately and highly exposed ones. In addition, exposure of peripheral blood lymphocytes to hydrogen peroxide or gamma-irradiation led to a similar degree of DNA damage and subsequent repair for all the studied populations.

Agricultural Workers' Diseases↗
PubMed2003

Biomonitoring with the comet assay of Greek greenhouse workers exposed to pesticides.

The pesticides in use in Greek greenhouses include a number of agents known to be mutagens and carcinogens. In the present study, we evaluated whether occupational exposure of agricultural workers to a complex mixture of pesticides resulted in a significant increase in DNA damage in human peripheral blood lymphocytes (PBLs). A total of 116 healthy individuals were divided into groups based on exposure to pesticides, smoking status, and gender. Alkaline comet assays performed on PBLs from these individuals indicated no statistically significant differences in basal DNA damage between the study groups. In addition, exposure of PBLs to a dose of hydrogen peroxide led to a similar degree of DNA damage and subsequent repair for all the study populations. The results of the study indicate that the agricultural workers who participated in this study had no detectable increase in DNA damage or alteration in the cellular response to DNA damage.

Adult↗
PubMed2002

Nicotinamide "protects" resting lymphocytes exposed to hydrogen peroxide from necrosis but not from apoptosis.

The aim of this work was to investigate the relationship between mechanisms of DNA repair and apoptosis induced by oxidative stress (H2O2) in human lymphocytes. Using the comet assay, fluorescent microscopy, and DNA electrophoresis, we studied the DNA damage induced by hydrogen peroxide (H2O2) treatment, the time and the amount of repair of strand breaks, the type of cell death, and the influence of inhibitors of repair (nicotinamide). When lymphocytes were treated with H2O2, we observed an increased in necrosis compared to apoptosis. However, when nicotinamide (which inhibits DNA repair) was added, the mode of death reversed to increased apoptosis. These results indicate that nicotinamide "protects" resting lymphocytes exposed to H2O2 from necrosis but not from apoptosis.

Apoptosis↗
PubMed2000

Effects of air pollution and smoking on DNA damage of human lymphocytes.

The comet assay is a useful technique for the study of genetic damage in humans exposed to environmental mutagens and carcinogens. In this study the effects of hydrogen peroxide (H(2)O(2)) and ultraviolet (UV) irradiation on 80 healthy individuals living in urban and rural areas with different smoking habits were investigated. Endonuclease III (endo III) treatment was also used to reveal the level of oxidized pyrimidine formation in these groups. The extent of damage and subsequent repair appear to be influenced by the living conditions (urban or rural areas). Smoking, however, was shown to have the most significant effect on DNA damage on all groups studied.

Adult↗
PubMed1998

Effects of smoking and aging on oxidative DNA damage of human lymphocytes.

The effects of H2O2-induced oxidative DNA damage in 80 healthy individuals with relation to age (20-25 and 55-60 years old) and smoking has been investigated with the comet assay technique. Both factors have shown a significant effect upon basal DNA damage with smoking appearing to have the most impact. A differentiation of the four groups response to induced oxidative damage was also observed. A distinctly separate behavior of the younger non-smokers group, when compared with the rest of the categories, was found. This is attributed to the lower degree of initial basal damage that occurs in their lymphocytes.

Adult↗
PubMed1997

Study of DNA damage induction and repair capacity of fresh and cryopreserved lymphocytes exposed to H2O2 and gamma-irradiation with the alkaline comet assay.

The alkaline SCGE assay was evaluated for use with cryopreserved lymphocytes in order to obtain results similar to the freshly isolated ones. The induction of DNA damage as well as the repair capacity of gamma-rays and H2O2 exposed cryopreserved human lymphocytes was found to be the same to that of the freshly isolated. Human lymphocytes (fresh or cryopreserved) responded differently to the effects of gamma-irradiation if compared to the H2O2 treatment. The distribution of DNA damage among gamma-irradiated lymphocytes was more homogeneous compared to H2O2, both in freshly isolated and in cryopreserved cells. 2.4 micrograms/ml phytohemagglutinin at the start of a 2-h incubation in RPMI of cryopreserved samples gave similar DNA repair and distribution patterns to the 2-h post-exposure incubation of freshly isolated lymphocytes. H2O2-induced DNA damage was not repaired completely. However, the repair of gamma-rays-induced DNA damage was more efficient. These findings confirm the different mode of action of the two agents on the induction of DNA damage, as well as, the different response of the lymphocytes' DNA repair system.

Cryopreservation↗
PubMed1995

Heavy metals enhance the reactivation of nitrous acid-treated adenovirus in HeLa cells.

Treatment of HeLa cells with cadmium chloride and zinc chloride increases the survival rate of nitrous acid-treated adenovirus 2 (ade2). This increase is maximal if the time interval between cell treatment and virus infection is delayed by 36 h. The induction process requires protein synthesis only during the 3-h period immediately following treatment; cycloheximide does not prevent the expression of enhanced reactivation if added to the cells after this time.

Adenoviruses, Human↗
PubMed1987

Enhanced reactivation of UV-irradiated adenovirus 2 is not associated with enhanced mutagenesis in carcinogen-pretreated HeLa cells.

Treatment of HeLa cells with low doses of the carcinogens aflatoxin B1, methyl methanesulfonate (MMS) or ethyl methanesulfonate (EMS) increases the survival rate of UV-irradiated adenovirus 2 (ade2). This increase is maximal if the time interval between cell treatment and virus infection is delayed by 36 h. No enhanced mutagenesis was found measuring the reversion frequency of a temperature-sensitive mutant of ade2 grown in HeLa cells treated with the same carcinogens. The enhanced viral reactivation observed does not, therefore, display a significant error-prone component.

Adenoviruses, Human↗
PubMed1985

Enhanced reactivation of UV-irradiated adenovirus 2 in HeLa cells treated with non-mutagenic chemical agents.

Treatment of HeLa cells with ethanol and sodium arsenite, compounds which are known to elicit the heat-shock response, before infection with UV-irradiated adenovirus 2 has been found to result in the enhanced reactivation of the damaged virus in a manner similar to that obtained by pre-irradiation or heating of the cells. Enhanced reactivation may be the result of the inhibition of DNA synthesis caused by these agents since hydroxyurea also produced a significant enhancement.

Adenoviruses, Human↗
PubMed1984

Heat-enhanced reactivation of UV-irradiated adenovirus 2 is not associated with enhanced mutagenesis in HeLa cells.

The reversion frequency of an adenovirus 2 temperature-sensitive growth mutant irradiated with different doses of UV light was determined after infection of control, UV-irradiated and heat-shocked HeLa cells. No enhancement of mutagenesis by treatment of the cells was observed. Heat-enhanced viral reactivation does not therefore display a significant error-prone component.

Adenoviruses, Human↗
PubMed1984

Hyperthermia enhances the reactivation of irradiated adenovirus in HeLa cells.

The reactivation of U.V.-irradiated adenovirus 2 in HeLa cells is enhanced 8-9 fold if the cells are given a brief hyperthermic shock before infection. Maximum reactivation is achieved by heating for 10 min at 45.5 degrees C and with a delay of 36 h between heating and infection. The induction process requires protein synthesis only during the 3 h period immediately following heating; cycloheximide does not prevent the expression of enhanced reactivation if added to the cells after this time. Heat-enhanced reactivation exhibits properties similar in some respects to radiation-enhanced reactivation and indicates an increased capacity of the heated cells to tolerate DNA damage.

Adenoviridae↗