Toxicology and Industrial Health最新文献

This study aimed to investigate the effects of high-frequency (6 GHz) radiofrequency electromagnetic radiation (RF-EMR) exposure on oxidative stress markers and kidney morphology. Our study was designed with 3 groups, each containing 10 animals. These groups were: control, sham, and RF-EMR exposed group. No treatment was applied to the control group; the sham group was housed in the same room under the same conditions and for equal periods of time, except that the generator was turned off. The RF-EMR exposed group was exposed to 6 GHz RF-EMR emitted from the signal generator for 4 hours per day for 6 weeks. At the end of the experimental period, intracardiac blood was collected from animals and plasma oxidant (MDA), antioxidant (SOD, CAT and GSH) and cortisol markers were analyzed. After, the rats in all groups were sacrificed and kidney tissues were removed. Hematoxylin and eosin staining methods were applied histopathologically. Blood-plasma GSH, CAT, SOD and MDA levels (excluding cortisol) were lower in the RF-EMR exposed group compared to the control and sham groups (p < .001). No significant difference was observed in plasma levels GSH, CAT, SOD, MDA and cortisol activities between control and sham groups. In addition, we reported that the histological characteristics of kidney tissue were affected by RF-EMR. The results of our study indicated that 6 GHz RF-EMR can function as an environmental stress factor and can modulate oxidative stress in blood plasma and cause morphological changes in kidney tissue.

Lead is one of the main environment pollutants, which has strong inhibitory effects on the functioning of the CNS. Exposure to high amounts of lead, even shortly, stimulates glial cells and activates inflammatory pathways in brain. Lead can also increase the amount of oxidative stress. In this study, the effect of hydrogen sulfide (H₂S) donors on lead-induced neurotoxicity was investigated. The protective effects of H₂S have been proven in various neurological diseases. Lead and H₂S were administered for 2 weeks. The animals' cognitive performance, exploratory behavior, and anxiety were evaluated using the shuttle box, open field, and elevated plus maze tests. The level of malondialdehyde (MDA), tumour necrosis factor alpha (TNFα), and interleukin 10 (IL-10); the total antioxidant capacity of the hippocampus; and blood lead levels were measured. Lead increased the level of TNFα and MDA and decreased the level of IL-10 in the hippocampus. H₂S was able to moderate the inflammatory and oxidative factors and tissue damage caused by lead in the hippocampus, which led to better cognitive and behavioral functions. The results of this study indicated that H₂S reduced the damage caused by lead through its well-known antioxidant and anti-inflammatory activity, which ultimately resulted in improved behavioral and cognitive functions in lead-poisoned animals. .

Formaldehyde (FA) is a critical industrial compound implicated in leukemogenesis via the induction of oxidative stress. Our previous studies observed aberrant expression of peroxiredoxin II (PrxII), phosphatase and tensin homologue (PTEN), phosphoinositide 3-kinase (PI3K), and protein kinase B (Akt) in FA-exposed bone marrow cells (BMCs) under conditions of oxidative stress. We speculate that the PrxII gene may be functionally linked to the PI3K pathway in formaldehyde-induced oxidative damage. Therefore, in the current study, we first used a specific PI3K inhibitor (LY294002, 10 μM) to suppress the PI3K pathway at 100 μM FA, and co-treated mouse bone marrow cells for 24 hours to investigate their potential interactions. We then evaluated the expression levels of PrxII, PTEN, PI3K, and Akt (via qRT-PCR and Western blot analysis), as well as the BMC's viability (CCK-8 assay), ROS levels (DCFH-DA), and cell apoptosis (Annexin V/PI staining). Additionally, to explore the potential regulatory role of PrxⅡ in the PI3K pathway, we employed siRNA-mediated PrxⅡ gene silencing through a small interfering RNA and subsequently measured PTEN, PI3K, and Akt mRNA and protein levels using qRT-PCR and Western blot analysis. We observed that inhibition of the PI3K pathway with 10 μM LY294002 mitigated FA-induced oxidative damage in BMCs, as evidenced by improved cell viability, reduced ROS levels, and decreased apoptosis rates. Moreover, PrxII silencing led to downregulation of PTEN expression while concurrently activating the PI3K/Akt signaling cascade. This study provides evidence that PrxII silencing may trigger the PI3K pathway mediated by PTEN gene, thereby exacerbating FA-induced oxidative injury.

Endosulfan is a broad-spectrum organochlorine pesticide widely used in many developing countries despite its high toxicity potential. Endosulfan, listed as potent endocrine-disrupting chemical and xenoestrogen, gains importance for its potential to cause reproductive and developmental dysfunction. In females, endosulfan disrupts ovarian and uterine development, leading to infertility, miscarriage, and developmental toxicity. It acts by mimicking estrogen and interferes with estrogen and androgen pathways, impacting hormone regulation and gene expression, including estrogen receptor α (ERα) and progesterone receptors. Endosulfan triggers oxidative stress in ovaries, reduces follicle count, and impairs uterine differentiation, affecting embryo implantation. Additionally, it alters gene expression and causes epigenetic modifications, contributing to reproductive dysfunctions. In males, endosulfan affects spermatogenesis by causing oxidative stress, mitochondrial dysfunction, and lipid peroxidation. It reduces sperm quality, motility, and quantity, with effects on testicular tissues, sperm chromatin condensation, and enzymatic activity. Oxidative damage, increased reactive oxygen species (ROS), and disrupted energy metabolism are central to its toxicity. Epidemiological studies also link pesticide exposure to reduced sperm counts, higher DNA fragmentation, and infertility. Moreover, endosulfan can cross the placental barrier, leading to fetal resorption, malformations, and maternal toxicity. This review provides a comprehensive overview of the reproductive toxicity of endosulfan in males and females. We also highlight the various possible mechanisms of reproductive toxicity of endosulfan and its potential to impart deleterious effects over HPG axis, gonads, and uterine differentiation and development and implantation.

Radiation exposures, whether planned or unexpected, can have harmful consequences on biological systems. To avoid these radiotoxic consequences, a variety of natural and synthetic radioprotectors are given prior to radiation exposure. The present study aimed to investigate the radioprotective potential of Aloe vera gel extract against damage induced by whole-body X-ray exposure in male balb/c mice. The animals were divided into four groups: Control, Aloe vera (50 mg/kg body weight orally on alternate days for 30 days), X-ray (cumulative dose of 2 Gy) (i.e., 0.258 Gy twice a day for four consecutive days) in the last week of the experimental protocol, and Aloe vera + X-ray. Following irradiation, Fourier transform infrared spectroscopy (FTIR) analysis showed structural changes in molecules by altering the ratios of CH₃/lipid, CH₂/lipid, lipid/protein, Amide I/II, and nucleic acid in liver and testes. X-ray exposure led to an increase in DNA strand breaks in the liver, spleen, kidney, and testes of mice, as indicated by comet assay. Bcl-2 levels were shown to be up-regulated in the kidney and testes following irradiation. In liver, kidney, and spleen, caspase 3 was also found to be up-regulated. Furthermore, after being exposed to X-rays, the expression of caspase 9 and bax was up-regulated in all the tissues examined. Administration of Aloe vera to the X-ray-exposed group exhibited decline in DNA strand breaks in all tissues investigated. Moreover, protein expressions of these genes were found to be down-regulated in the Aloe vera + X-ray-exposed group. These observations illustrate the potential of Aloe vera in providing radioprotection for rodents, possibly DNA protection, through its anti-apoptotic properties.

This study examined ingredient disclosure and concealment patterns in cosmetic products reported under California's Safe Cosmetics Program (CSCP), with particular attention to trade secret designations and their implications for public health transparency. Drawing on a dataset from CSCP filings, descriptive analyses and logistic regressions were calculated to identify category predictors of ingredient non-disclosure, including product type, manufacturer characteristics, and chemical hazard profiles. Limitations in standard statistical models, such as rare outcomes and complete separation, required a pivot to stratified descriptive summaries and sensitivity checks. The study also documented inconsistencies in ingredient naming conventions and reporting formats that hinder public access and regulatory oversight. The results highlight the need for stronger disclosure standards, improved data coordination, and stronger labeling enforcement to enable meaningful assessment of chemical risks in personal care products. The analysis provides a framework for translating legal disclosure mandates into empirical research and policy evaluation.

Occupational exposure to volatile organic solvents has been reported to lead to hazardous effects. Ethyl acetate is a volatile organic compound used commonly in industry and found in many commercial products. The present study aimed to investigate the acute behavioural effects of ethyl acetate exposure in rats. The mechanism of its effects was further investigated by focusing on the possible involvement of L-type calcium channels. For this purpose, ethyl acetate (0.3 g/kg, i.p.) alone or concurrently with nimodipine (3 and 5 mg/kg, i.p.), a dihydropyridine calcium channel antagonist selective to L-type calcium channels, was administered to male Wistar albino rats. When compared to the saline control group, ethyl acetate significantly decreased the number of square-crossing, rearing, and sniffing in the open-field and impaired the reference memory performance in the three-panel runway. However, administration of nimodipine at the given doses did not block these effects of ethyl acetate. The findings suggest that L-type calcium channels may not contribute to the mechanism(s) responsible for the acute toxicity of ethyl acetate in rats regarding their central nervous system depression and memory disturbances although it should be more thoroughly investigated in further studies.

Cadmium (Cd) is a toxic environmental heavy metal with a long biological half-life and a high affinity for renal accumulation, posing serious health risks in both humans and animals. Ursodeoxycholic acid (UDCA), a bile acid primarily used for liver disorders, has gained attention for its antioxidant properties and potential protective effects in various toxicological settings. This study investigated the protective role of UDCA against cadmium-induced renal injury in rats. Twenty-eight male Wistar Albino rats (180-220 g) were divided into four groups: control (C, n = 6), cadmium (Cd, n = 8), UDCA (n = 6), and cadmium + UDCA (Cd + UDCA, n = 8). Cd was administered intraperitoneally (3 mg/kg) from days 8 to 15. UDCA was given intragastrically (60 mg/kg) from days 1 to 15. The Cd + UDCA group received both treatments concurrently. Biochemical analysis showed that Cd exposure significantly elevated serum BUN, creatinine, KIM-1, and MDA levels while decreasing GSH concentrations, indicating oxidative stress and renal injury. Conversely, the Cd + UDCA group demonstrated marked attenuation of these changes, with significantly lower BUN, creatinine, KIM-1, and MDA levels, and partially preserved GSH levels. Histopathological examination confirmed extensive renal damage in the Cd group, including cortical necrosis, tubular debris, vascular damage, glomerular alterations, and interstitial inflammation. These alterations were less severe in the Cd + UDCA group, supporting the biochemical findings. In conclusion, UDCA partially mitigated cadmium-induced oxidative stress and nephrotoxicity, reducing renal injury and supporting its potential as a protective agent against heavy metal-induced kidney damage.

Potassium bromate (KBrO₃), a strong oxidizing agent, is widely used in various industrial settings, thereby increasing the risk of oxidative damage and subsequent tissue toxicity in individuals who are exposed to it. Additionally, KBrO₃ has been used as a maturing agent and is also generated as a by-product during water disinfection process. Previously, we have demonstrated that KBrO₃ causes oxidative damage to human erythrocytes. The present work shows the protective effects of taurine (2-aminoethane sulfonic acid) against oxidative stress induced by KBrO₃ in human erythrocytes. Erythrocytes from healthy donors were incubated with either KBrO₃ alone or taurine alone and KBrO₃ plus varying concentrations of taurine. The treatment of erythrocytes with KBrO₃ caused disruption in the oxidative-reductive homeostasis as evidenced by severe alterations in antioxidant enzyme functions and a marked depletion in total sulfhydryl content. Exposure of erythrocytes to KBrO₃ also caused the elevation in methemoglobin levels, protein carbonyls, hydrogen peroxide levels, protein oxidation, and lipid peroxidation. However, the KBrO₃-induced cellular/biochemical alterations were greatly protected by taurine. These results suggest that taurine significantly decreases the toxic effects of KBrO₃ in human erythrocytes.

Hydrogen peroxide (H₂O₂) is a well-known irritant that affects the eyes, respiratory tract, and skin, and long-term exposure may lead to chronic respiratory conditions such as bronchitis, pulmonary fibrosis, and an increased risk of lung cancer, particularly in occupational settings. The objective of this study was to evaluate occupational exposure to H₂O₂ among dairy processing plant workers and to characterize the associated semi-quantitative risks using the methodology of the Singapore Occupational Health Department. This research was conducted in the sterilization units of three dairy processing plants located in Neyshabur, Iran. The semi-quantitative risk assessment in this study adhered to the methodology recommended by the Singapore Occupational Health Department. The findings revealed that the average occupational exposure to H₂O₂ for 29 workers across three dairy processing plants was 0.91 ± 0.54 ppm, with individual exposure levels ranging from 0.10 to 2.12 ppm. The mean exposure level exceeded the adjusted threshold limit value (TLV) for H₂O₂ (0.78 ppm). The evaluation of health risks associated with H₂O₂ exposure revealed that all participants fell within the medium-risk category. This classification underscores the potential for adverse health effects among dairy workers and highlights the need for targeted interventions to mitigate exposure risks and enhance workplace safety.