Iranian Journal of Toxicology
Volume:16 Issue: 4, Oct 2022

Nickel is a carcinogenic, heavy metal released through industrial activities and via natural resources. It is able to cause DNA damages by reducing the efficiency of DNA repair mechanisms. However, the exact time point at which it is able to interfere with these mechanisms is not yet clearly understood.

To find the most nickel-vulnerable time of repair mechanisms, human dermal fibroblasts (HDF) were treated with three doses of nickel before and after X-irradiation. The induced frequency of chromosomal abnormality was studied using micronucleus assay in binucleated cells. The cytotoxicity of different treatments was established using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.

The results revealed that nickel treatment had a synergistic effect on inducing Micronucleus frequency only when cells were treated 2 hours before X-irradiation. The X-ray treatment of the cells with 5 and 10 mM nickel had a cytotoxic effect mainly when given 6 hours after the irradiation.

The results suggest that nickel can interfere with human DNA repair mechanisms only at the start of the process, while having no significant effect on the human DNA repair mechanisms when activated.

Long-term use of levofloxacin can cause alterations in the liver function. This study aimed to determine the protective effect of black seed oil (BSO) against liver injury due to levofloxacin administration in rats.

The chemical composition of BSO was analyzed with gas chromatography and mass spectrophotometry (GC-MS). Rats (n=30) were treated daily with levofloxacin and BSO at three doses (1, 2 or 4 mL/kg) orally for 28 days. The presence of liver injury was determined based on serum biomarkers and liver malondialdehyde (MDA) levels, and histopathological examinations. 

The GC-MS analyses showed that BSO contained 25 chemical compounds, including thymoquinone (10.14%). The levofloxacin administration significantly increased the liver enzymes and MDA levels, and induced a marked alteration in the liver histological structures. Treatments of rats with one or two mL/kg BSO significantly decreased the liver enzymes, and MDA levels compared to those that received levofloxacin alone (P<0.05). However, the highest dose (4 mL/kg) BSO failed to improve liver MDA levels. The recovery of liver histological damages was also observed in rats treated with BSO. 

It was concluded that the BSO administration reduced the liver dysfunction due to levofloxacin at doses of 1 or 2 mL/kg, but not at 4 mL/kg. Further research is warranted to explore if the protective effect of BSO is associated with its antioxidant properties.

Neem leaves (Azadirachta indica L.) have been used for many therapeutic purposes and medicinal applications. The extract of this plant has been used in both male and female genders as a traditional agent to prevent early pregnancy. In this study, the effect of this extract was investigated histologically and morphometrically on the germinal epithelia of the seminiferous tubules, epididymis and secretory epithelia of rats’ prostate glands.

Twenty male albino rats were divided into four groups of five each and administered the extract at a concentration of zero, 100, 200 or 400 mg/kg of the body weight for 50 consecutive days. These rats were sacrificed and the male reproductive organs were removed, weighed and processed for routine histological examinations. The micrographs were analyzed and the structural changes in the epithelial lining and morphometric analyses were recorded, which included measuring the epithelial thickness in the seminiferous tubules, epididymis and secretory prostatic epithelia.

The extract was found to reduce the rats’ weight; decreased both the weight and dimension of the testes; reduced the number of germinal epithelial lining cells in the seminiferous tubules of the testes, the epididymal and prostatic secretory epithelial cells.

The histological alterations were most significant in response to the treatment with the extract at 200 mg/kg of the rats with the greatest damages observed in the epithelial lining. The deleterious effects of the extract were found to be dose-dependent and this corroborates the use of this extract as a contraceptive in animal models, and potentially in humans.

Studies suggest that sulfur may react with plants or monocellular organisms, such as fungi, to produce toxic agents. It has been theorized that sulfur enters cells and affects their respiration. This study reports on a phototroph development that leads to the diminution and/or production of sulfur and release of hydrogen sulfide from public ponds.

This study was conducted in anoxic stabilization ponds at a dimension of 1×0.25×1 (m), with a hydraulic retention time of 6 days. The ponds’ water was tested during the dark and light cycles. The experiments were carried out by factorial design and measured three variables: volumetric organic loading, sulphate concentrations and temperature.

Cyanobacteria and Rhodobacter species were the most abundant phototroph cellular organisms. The mean value of total sulfur and un-ionized hydrogen sulfide concentration were 74 mg/L and 21 mg/L, respectively, at the volumetric organic loading of 100 g BOD5/m3 per day. The efficiencies of biochemical and chemical oxygen removal were 71.9% and 59.1%, respectively. The mean proliferation rate of photosynthetic sulfur bacteria was 3.4×106 cells/ml.

photosynthetic sulfur bacteria significantly reduced the sulfur concentration generated in the ponds. The illumination of bright light enhanced the sulfur reduction by the photosynthetic sulfur bacteria in the wastewater of the anoxic stabilization ponds.

Poisoning with carbon monoxide occurs occasionally worldwide, and the gold diagnostic standard is to measure carboxyhemoglobin level in the blood. This study investigated the correlation between carboxyhemoglobin and the end-tidal carbon dioxide levels in 50 patients with carbon monoxide poisoning.

We recruited 50 volunteer patients who had been admitted to the Emergency Services of Istanbul Medipol University Hospital between January 2017 and January 2018. They had been diagnosed with carbon monoxide poisoning unrelated to fire accidents. The arterial and venous blood gases, and other blood and clinical parameters were also measured. The patients’ end-tidal carbon dioxide levels were measured from the nose and mouth air, using a Capnostream 20p bedside monitor. Pearson’s correlation analyses were performed and the results were compared with the end-tidal carbon dioxide, carboxyhemoglobin and oxygen saturation in the arterial and venous blood samples.

The Mean±SD age was 33.98±10.89 years. The Mean±SD arterial and venous carboxyhemoglobin values were 18.05±7.10 and 12.11±9.67, respectively. There were no statistically significant differences between the oxygen saturation, and the arterial and venous blood levels of carboxyhemoglobin (P=0.870, P=0.950), respectively. Also, no statistically significant correlations were found between the end-tidal carbon dioxide, and the arterial and venous carboxyhemoglobin levels (P=0.529, P=0.601), respectively.

The results from the blood analyses demonstrated that there was no statistically significant difference between the end-tidal carbon dioxide and the carboxyhemoglobin levels in these patients who had been earlier diagnosed with carbon monoxide poisoning, unrelated to fire accidents.

Bleaching teeth is popular because the discoloration is a major people’s concern. This study aimed to compare the effect of three antioxidants on the microleakage of composite resin filling after bleaching teeth with 35% H2O2, thus minimizing the potential clinical toxicity of filling materials entering patients’ body.

Sixty-six extracted intact teeth were included in this study. After preparation of a ClV cavity on the buccal surface, the teeth were randomly divided into six groups (n=11, each). Except for group A (control), all others were bleached. Cavities in group A were filled with composite resin. In group B, the samples were immediately restored after bleaching while in group C, the filling was delayed for two weeks after bleaching. In groups D, E, and F, the cavities were treated with either sodium ascorbate, ascorbic acid, or vitamin C, and the filling restored. Teeth were sectioned and the microleakages examined microscopically, and the data were analyzed statistically.

Group A showed the least amount of microleakage. In Group B, there was a significant increase in the microleakage when the samples were filled immediately after bleaching. The microleakages among groups of C, D, E, and F were similar to those in group A.

The microleakage increased significantly after bleaching with 35% H2O2, while treating dental cavities with the antioxidants effectively reduced the microleakage. Thus, delayed filling is a useful approach to minimize the microleakage. The findings help reduce or prevent the clinical toxicity arising from the microleakage of filling materials.

Studies suggest that herbal remedies may serve as functional anti-diabetic agents. This study investigated the therapeutic role of Calotropis procera aqueous-methanol root extract in hyperglycaemic and hepatopathy disorders in Wistar rats after exposure to alloxan. This compound destroys pancreatic β-cells and produce diabetes in experimental animals. 

Spectrophotometric methods were used to assay the antioxidants and biochemical parameters while histological examinations were employed to assess the structural changes in the harvested tissue under light microscopy.

The secondary metabolites were quantified by spectrochemistry methods. The extract was rich in flavonoids and low in terpenoids, and contained ursolic acid, lupeol and oleanolic acid. The extract’s strong anti-radical activity was due to its low IC50 values. The extract suppressed α-amylase more than α-glucosidase activity by 3.99%, and the blood glucose declined in the diabetic group by 64.25%. The malondialdehyde level was low in the treated group while it declined significantly in the normal group. The superoxide dismutase, catalase and glutathione levels were also low in the untreated versus the treated group. There were reduced activities of aspartate and alanine aminotransferases and alkaline phosphatase; however, the albumin and total protein levels increased mildly in the treated compared to the untreated group. The liver and pancreas histology revealed normal hepatocyte and β-islet architecture in the treated group as opposed to blood vessels congestion and β cells necrosis in the untreated group.

The extract's anticytotoxic effects may be linked to the antioxidant role of its phytochemical constituents.

Dyslipidemia constitutes a serious public health concern globally. It has been established that excessive fructose intake results in dyslipidemia; however, whether dexamethasone aggravates or alleviates fructose-induced dyslipidemia is unknown. Thus, we examined the effects of dexamethasone on dyslipidemia and hyperuricemia in high fructose-taking Wister rats. 

Twenty male Wister rats were randomly grouped as control (distilled water), fructose (10% fructose w/v), dexamethasone (0.2 mg/kg, PO) and fructose+dexamethasone. After a 21-day exposure, the serum and heart samples were harvested, processed and analyzed for biochemical assays.

Our findings reveal that exposure of rats to high fructose significantly increased blood glucose, elevated serum triglycerides and uric acid, activity of xanthine oxidase, and lowered high density lipoprotein cholesterol (HDL) level. However, dexamethasone administration had no significant effect on the blood glucose and did not alter the serum levels of triglycerides, uric acid and xanthine oxidase. Meanwhile, both fructose and dexamethasone treatments independently elevated the serum levels of total cholesterol (TC), low density lipoprotein cholesterol (LDL) and malondialdehyde. Further, the fructose treatment elevated the TG/HDL ratio, while both fructose and dexamethasone treatments individually and synergistically elevated TC/HDL ratio. Our study also showed that co-administration of fructose and dexamethasone aggravated the elevated serum levels of TC and LDL, while it impaired the enzymatic antioxidant systems.

Dexamethasone, though slightly reduced fructose-induced hyperglycemia, impaired the antioxidant enzymes and escalated dyslipidemia during fructose intake. Hence, our study suggests that dexamethasone administration may increase the risk of CVD in animals with excessive intake of fructose.