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Showing 4 results for Toxicity
Review of Phthalates Exposure and Toxicity
Samaneh Taghilou, Mirjamal Hosseini,
Volume 3, Issue 2 (10-2015)
Abstract

The dialkyl- or alkyl/aryl esters of 1, 2-benzenedicarboxylic acid, which are known as Phthalates, are high-production volume synthetic chemicals and considered as environmental pollutants, due to high production and uses in community, plastics industry and common consuming products. Di-(2-ethylhexyl) phthalate (DEHP) is the most abundant phthalate in the environment. Human exposure with DEHP could be done via different chemical compounds including food packaging, household furnishings, nutritional supplements, cleaning materials and insecticides. Besides, exposure of human with phthalates occurs through different pathways such as direct contact and using Phthalate-containing products, and indirectly through leaching into other products, or general environmental contaminations. Historically, the diet has been considered the major source of phthalate exposure in the general population, but in all sources, pathways, and their relative contributions to human exposures are not well understood. Medical devices are other source of significant exposure in human. Furthermore, cosmetics, personal care products, pharmaceuticals, nutritional supplements, herbal remedies and insecticides, may result in significant but poorly quantified human exposure with this compounds. In the present review article, we tried to discuss about metabolism of phthalates in human, toxicity, monitoring of phthalates in foods, environment, and cosmetic products and then metabolites of phthalates. Finally, evaluation of human exposure through biological control is discussed.


The Simultaneous Effect of Linum Usitatissimum Supplementation and Aerobic Training on 6-Methylguanine and ATP in the Endothelial Aorta and Heart Tissues in Rats Poisoned with H2O2
Seyed Mostafa Rezaei, Bahram Abedi, Hoseyn Fatolahi,
Volume 9, Issue 3 (10-2021)
Abstract
Background and Objective: As a high-energy demanding tissue, the heart is exposed to a high level of ROS molecules such as H2O2, leading to cardiovascular disorders through damaging macromolecules such as DNA and disrupting ATP production. Hence, this study aimed to investigate the simultaneous effect of aerobic exercise (Ae) and Linum Usitatissimum (Lu) supplementation on DNA damage and ATP synthesis in heart and aorta endothelial tissues in rats poisoned with hydrogen peroxide (H2O2).
Material and Methods: 56 male Wistar Albino rats were randomly divided into 7 groups, including HC (Healthy Control), TC (Toxicated Control), Lu1 (Received 5 mg/kg of Lu), Lu2 (Received 10 mg/kg of Lu), Ae (Received only Aerobic Exercise), Ae Lu1, and Ae Lu2. Then, all groups got poisoned by H2O2 except HC. Next, they received Linum Usitatissimum (Lu) supplementation and Low-Intensity Interval Training (LIIT). Finally, 24h after the last treatment session, the level of 6-methylguanine (6MG) and ATP were measured via the ELISA technique in cardiovascular tissue.
Results: The findings determined that Lu supplementation and Ae significantly diminish the 6-methyl guanine level in endothelial (F=111.3, p=0.0008, ƞ=0.9823) and heart cells (F=147.9, p=0.0005, ƞ=0.9867). Also, the ATP level was increased significantly in endothelial (F=342.6, p=0.0003, ƞ=0.9942) and heart cells (F=135.1, p=0.0013, ƞ=0.9854). However, no considerable changes were found for both factors in groups who received Ae or Lu singularly.
Conclusion: The study showed that concurrent administration of Lu and Ae could exert dynamic cardioprotective properties through their antioxidant effects.

Anticancer Activity of Doxorubicin Loaded PBMA-b-POEGMA Micelles against MCF7 Breast Cancer Cells and HepG2 Liver Cancer Cells
Hamideh Gharnas-Ghamesh, Mojtaba Masoumi, Vahid Erfani-Moghadam,
Volume 9, Issue 3 (10-2021)
Abstract
Background and Objective: Cancer is one of the most serious diseases. Doxorubicin is a type of chemotherapy drug used to treat a variety of cancers. Doxorubicin is a type of chemotherapy drug used to treat a variety of cancers. However, its side effects have limited its use. The aim of this study was to synthesize and evaluate polymer micelles containing doxorubicin and evaluate its toxicity on MCF7 breast cancer cells and HepG2 liver cancer cells.
Material and Methods: For this purpose, PBMA-b-POEGMA diblock copolymer was first synthesized using the RAFT method and confirmed by GPC. Dynamic light scattering (DLS) and Transmission electron microscope (TEM) were used to observe the morphology, size, and polydispersity of the micelles. In addition, in vitro cytotoxicity of DOX-loaded polymeric micelles against MCF7 cells and HepG2 cells were assessed. Furthermore, cell uptake and apoptosis assay of DOX-loaded polymeric micelles against MCF7 cells were evaluated.
Results: The TEM image revealed that the nanoparticles were spherical and uniform. The particle size and polydispersity measured by DLS were 35 nm and 0.13, respectively. The drug encapsulation efficiency and drug loading contents were 50±3.46 % and 4.53±0.29 %, respectively. The drug release rate was reported 69% in saline phosphate buffer (pH 7.4) within 24 hours. The results showed that micelles containing doxorubicin had a greater effect on MCF7 cell viability than the free drug. The MTT assay demonstrated that micelles were biocompatible to HepG2 cells while DOX-loaded micelles showed significant cytotoxicity. The IC50 of doxorubicin-loaded micelles against MCF7 cells were obtained to be 0.5 μg/ml. It was further shown that micelles containing doxorubicin had higher cell uptake and apoptosis than free drugs on MCF7 cells.
Conclusion: These polymeric micelles are an ideal candidate to deliver anticancer agents into breast cancer cells.

Cytotoxic effects of I3C and TCDD on macrophages: Role of aryl hydrocarbon receptor target genes
Delara Omrani , Saeed Mohammadi , Yaghoub Yazdani ,
Volume 13, Issue 4 (12-2025)
Abstract
Background: Macrophages are central effectors of innate immunity and exhibit remarkable functional plasticity in response to environmental stimuli. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that plays a critical role in regulating macrophage function, immune homeostasis, and xenobiotic metabolism. Two well-characterized AhR ligands, indole-3-carbinol (I3C), a dietary phytochemical derived from cruciferous vegetables, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a persistent environmental pollutant, exert divergent biological effects despite engaging the same receptor. However, their differential cytotoxic impact on macrophages and the extent to which they activate downstream AhR target genes remain poorly characterized. This study aimed to evaluate and compare the cytotoxic effects of I3C and TCDD on THP-1-derived macrophages and to assess the consequent transcriptional regulation of three canonical AhR target genes: CYP1A1, CYP1B1, and AhRR.
Methods: THP-1 human monocytic cells were differentiated into macrophages using phorbol 12-myristate 13-acetate (PMA) and 2-mercaptoethanol (2-ME). Differentiated macrophages were treated with I3C (10 ng/µL) or TCDD (100 nM), each dissolved separately in dimethyl sulfoxide (DMSO), for 24 and 48 hours. Lipopolysaccharide (LPS; 100 ng/mL) was used as a positive control. Cell viability was assessed using the MTT colorimetric assay. Gene expression of CYP1A1, CYP1B1, and AhRR was quantified by real-time quantitative RT-PCR (qRT-PCR) using SYBR Green chemistry, with GAPDH as the reference gene. Data were analyzed by one-way ANOVA followed by Tukey’s post-hoc test; significance was set at P-Value < 0.05.
Results: TCDD demonstrated pronounced cytotoxicity, reducing cell viability by 25% at 24 hours (P-Value < 0.05) and by 40% at 48 hours (P-Value < 0.01) compared to untreated controls. I3C induced significantly milder cytotoxicity, with viability reductions of 10% and 15% at 24 and 48 hours, respectively (P-Value < 0.05). DMSO vehicle control did not significantly affect cell viability. Real-time qRT-PCR analysis revealed that both ligands significantly upregulated CYP1A1, CYP1B1, and AhRR. TCDD induced greater upregulation of CYP1A1 (5.5-fold at 48 h) and CYP1B1 (4.8-fold at 48 h) compared to I3C (3.2-fold and 2.7-fold, respectively; P-Value < 0.05 for all between-group comparisons). AhRR was upregulated to a similar extent by both ligands (~2.1-fold).
Conclusion: TCDD exhibited markedly higher cytotoxicity than I3C in THP-1-derived macrophages, consistent with potent and sustained AhR activation. I3C induced comparatively milder cytotoxic and transcriptional responses, suggesting more controlled AhR engagement. These results provide mechanistic insights into ligand-dependent AhR signaling in macrophages and underscore the immunotoxicological risks of TCDD exposure, while highlighting I3C as a candidate for future anti-inflammatory research.

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