Journal of Applied Toxicology

Systematic Review of the Epidemiology of Hair Relaxer Use and Hormone‐Sensitive Reproductive Outcomes Among Black Adult Women in the United States

ABSTRACTHair relaxers are predominantly used by Black women in the United States. It has been recently suggested that exposure to potential endocrine‐disrupting compounds from the use of these products may be associated with the development of gynecological and breast cancers and anatomically relevant nonmalignancies. We conducted a systematic literature review using PubMed to identify original studies reporting measures of association between hair relaxer use and relevant adverse outcomes, focusing specifically on Black women in the United States. A total of 1382 studies were initially identified, and after consideration of the exclusion and inclusion criteria, the final set of studies consisted of seven cohort studies and one case–control study. The overall findings suggest that Black women in the United States do not experience an increased risk of breast cancer, ovarian cancer, or uterine cancer due to hair relaxers. One study found a statistically significant association between hair relaxer use and uterine leiomyomata, but there were no other studies identified to support these findings. None of the studies characterized the chemical constituents of hair relaxers. From an epidemiologic perspective, the weight of the evidence does not support the hypothesis that the use of hair relaxers is a risk factor for gynecological and breast cancers in US Black women.

Fructose‐1,6‐bisphosphate induces generation of reactive oxygen species and activation of p53‐dependent cell death in human endometrial cancer cells

AbstractFructose‐1,6‐bisphosphate (F1,6BP), an intermediate of the glycolytic pathway, has been found to play a promising anticancer effect; nevertheless, the mechanisms involved remain poorly understood. The present study aimed to evaluate the effect and mechanisms of F1,6BP in a human endometrial cancer cell line (Ishikawa). F1,6BP showed an antiproliferative and non‐cytotoxic effect on endometrial cancer cells. These effects are related to the increase in reactive oxygen species (ROS) levels and mitochondrial membrane potential (ΔΨm). These harmful stimuli trigger the upregulation of the expression of pro‐apoptotic genes (p53 and Bax), leading to the reduction of cell proliferation through inducing programmed cell death by apoptosis. Furthermore, F1,6BP‐treated cells had the formation of autophagosomes induced, as well as a decrease in their proliferative capacity after withdrawing the treatment. Our results demonstrate that F1,6BP acts as an anticancer agent through the generation of mitochondrial instability, loss of cell function, and p53‐dependent cell death. Thus, F1,6BP proves to be a potential molecule for use in the treatment against endometrial cancer.

Pitavastatin induces caspase‐mediated apoptotic death through oxidative stress and DNA damage in combined with cisplatin in human cervical cancer cell line

AbstractPitavastatin (PITA) is a 3‐hydroxy‐3‐methylglutaryl‐CoA (HMG‐CoA) reductase inhibitor to treat hypercholesterolemia and in recent studies is focused that its potential anti‐cancer effect. This study was aimed to elucidate the effect of PITA alone and in combination with cisplatin on cervical cancer cells (HeLa) in vitro. Cytotoxicity of PITA (5–200 μM) was evaluated by 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) and neutral red uptake (NRU) assays for 24, 48, and 72 h. Cell apoptosis and cell cycle analyses were performed in flow cytometry (0.1–100 μM). The evaluation of genotoxic effects and oxidative DNA damage of PITA (2–200 μM) were performed with standard comet assay, formamidopyrimidine glycosylase (fpg)‐modified comet assay, and reactive oxygen species (ROS) activation in HeLa cells. PITA alone reduced cell viability in a dose‐dependent manner (20–200, 20–200, and 5–200 μM for 24, 48, and 72 h, respectively, in MTT). The combined treatment of PITA with cisplatin resulted in significantly greater inhibition of cell viability. ROS and DNA damage increased significantly at 100 μM for 4 h and 20 μM for 24 h, respectively. PITA‐induced apoptosis, an increased proportion of sub G1 cells, was monitored, and also, it increased the expression of active caspase‐9 and caspase‐3 and upregulated cleaved poly adenosine diphosphate ribose polymerase (PARP) by western blotting and caspase 3/8/9 multiple assay kit. We conclude that PITA can be used to efficiently cervical cancer studies, and promising findings have been obtained for further studies.