To unveil the role of reactive oxygen species (ROS) and antioxidants in signaling and involvement in cancer progression and therapy.Background: Cancer is considered one of the main causes of mortality in developed countries and expected to be more in developing countries as well. Although some cancers may develop at young age, yet almost all types of cancers are an accumulation of genetic and epigenetic cell damages. Cancer is considered a diverse collection of diseases on a cellular level rather than a single disease; and each disease has a different cause as well. ROS have been seen as harmful toxic molecules; however, they are recognized for cellular signaling capabilities. Elevated levels of ROS have protumorigenic activities; they induce cancer cell proliferation, and adaptation to hypoxia in addition to other effects like DNA damage and genetic instability.They are produced excessively by cancer cells to hyperactivate cellular transformation meanwhile increasing antioxidant capacity to avoid cell death.Methods: We discussed peer reviewed published research work from 1987 to 2021. In this paper, we review the role of antioxidants as defensive barrier against excessive ROS levels for maintaining oxidationreduction (redox) balance; however, antioxidant can also strive in tumor cells with their scavenging capacities and maintain protumorigenic signaling and resist the cancer cell oxidative stress and apoptosis. High doses of antioxidant compounds could be toxic to cells as they are capable of reacting with the physiological concentrations of ROS present for normal cellular processes and signaling.Conclusions: Maintaining cellular redox homeostasis is vital for healthy biological system. Therefore, therapeutic modalities for cancer including antioxidants and ROS management should be used at certain doses to target specific redox pathways involved in cancer progression without disrupting the overall redox balance in normal cells.

The results of our study demonstrated a tendency toward altered distribution of lipoprotein subclasses in favor of more proatherogenic particles in childhood hypertension. Also, hypertensive obese children had increased proatherogenic CETP activity.

Background/aim: Juvenile obesity is associated with several metabolic abnormalities, one of them being atherogenic dyslipidemia. Suboptimal fetal growth is associated with obesity risk in childhood, but also with increased rate of metabolic diseases in later life. This study investigated associations of neonatal data (Apgar score, birth weight and birth length) with low-density lipoprotein and highdensity lipoprotein (LDL and HDL) subclasses in a group of obese children, as well as a possible impact of breastfeeding duration on obesity-associated lipoprotein subclasses distributions. Materials and methods:We included 42 obese children, aged 14.2 ± 2.1 years. LDL and HDL subfractions were separated by gradient gel electrophoresis and biochemical parameters were assessed by routine methods.Results: Compared with obese children with Apgar ≥ 9, the group with Apgar < 9 had significantly higher percentages of small, dense LDL particles (P < 0.05), due to reduced LDL I (P < 0.01) and increased LDL III subclasses (P < 0.05). Birth weight was positively associated with the proportions of LDL I particles (P < 0.001), whereas birth height positively correlated with the amount of HDL 2b subclasses (P < 0.05). The group of never or less than 3 months breastfed children had significantly smaller LDL size (P < 0.01) and lower proportion of HDL 2a particles (P < 0.05) than their ≥3 months breastfed peers. Conclusion:The results showed significant associations of neonatal characteristics with LDL and HDL particle distributions in obese children. In addition, our results point toward positive aspects of longer breastfeeding duration on lipoprotein particle distributions in obese children.

Peracetic acid (PAA) and hydrogen peroxide (H 2 O 2 ) were more potent at pH 8.2, while linear alkylbenzene sulfonate (LAS) showed higher potency at pH 5.0 against Pseudomonas fluorescens ATCC 13525. The aim was to understand the changes in the cellular redox status, ultrastructure and morphology underlying the synergistic bacterial control effects of selected pH values alone and treatments. The minimum inhibitory concentrations of PAA and H 2 O 2 at pH 8.2, and MIC of LAS at pH 5.0 were tested during the stationary growth phase of planktonic cells. pH 8.2 alone mainly elevated the protein carbonyls level and decreased the levels of low molecular weight thiols (LMWT), which could potentiate the effect of H 2 O 2 and PAA, while pH 5.0 alone largely decreased the total thiol level that could facilitate LAS action. Free radicals were only detected with LAS and PAA treatments. H 2 O 2 and PAA increased the levels of protein carbonyls, while reduced LMWT levels. LAS increased the levels of protein carbonyls, while reduced the total thiol level. H 2 O 2 , PAA and LAS were also found to increase SOD and decrease catalase specific activities. Each treatment showed distinct alterations and disruption in cytoplasmic structures. We suggest that exposing bacteria to the test oxidants and LAS at the selected pH ranges resulted in high generation of reactive species which activated complex oxidative processes and antioxidant defense pathways causing an imbalance of the cellular redox homeostasis that led to deformity and collapse of ultrastructure at late stage of oxidative damage, and eventual control of bacterial growth.