Iranian Journal of Toxicology
Volume:18 Issue: 3, Jul 2024

Colon cancer is one of the most prevalent malignancies in both men and women. This study investigated the anticancer efficacy of a new synthetic form of quinolone nanoparticles (QNPs) against colon cancer cells. As an experimental model, we investigated methods to prevent the development of colon cancer in adult male albino rats induced by 1,2-dimethylhydrazine (DMH).

Forty adult male rats (weighing 150-200 g) were randomly assigned to four groups of ten as follows:Group 1: Normal rats considered the reference group.Group 2: Normal rats treated intraperitoneally with 100 μg/kg/day of quinolone.Group 3: Rats with induced colon cancer by DMH.Group 4: Rats with colon cancer, as the experimental model, and administered QNPs at 100 μg/kg/day for 6 weeks.

The results showed that QNPs significantly improved the treatment of induced colon cancer in rats. This finding was supported by significant increases in CD4, colon SOD, and GPx activity, as well as in GSH and CAT levels. Further discoveries included a significant decline in the serum values of CEA, CA19-9, AFP, TNF-α, IL1β, ALT, AST, urea, creatinine, cholesterol, triglycerides, colon DNA damage, MDA, and NO. The histopathological results demonstrated the therapeutic potential of QNPs, which were successful in halting the development of colon cancer in an experimental animal model.

The findings of the current study demonstrated that QNPs were able to prevent colon cancer in rats by enhancing their immune system, lowering inflammatory markers, and improving damaged oxidative stress tolerance.

The human race is currently burdened with cases of multi-drug-resistant pathogenic microorganisms, causing a menace to the efficacy of the existing antimicrobials. This has created a critical need for innovative drugs with minimal toxicity. The present study aimed to assess the sub-chronic toxicity of some transition metal complexes containing Schiff base ligand with 2,2-bipyridine.

A total of 36 male rats weighing 178.12±5.48 g were assigned to six groups of six per group. Group A: administered 5% DMSO; Group B: treated with 200 mg kg-1 BW of 2, 2-Bipyridine; Group C: treated with 200 mg kg-1 BW MPK-TSC; Group D: treated with 200 mg kg-1 body weight [Cu (MPK-TSC) (Bipy)Cl2]; Group E: treated with 200 mg kg-1 BW [Ni (MPK-TSC) (Bipy)Cl2]; and Group F: treated with 200 mg kg-1 BW [Zn (MPK-TSC) (Bipy)Cl2]. Blood was collected via cardiac puncture for hematological analysis. Liver and kidney homogenates were used for plasma enzymes, liver and renal functions, and the antioxidant indices. The histological sections of rats' liver and kidney tissue samples were also examined.

Animals from the control and different treated groups exhibited normal body weight gain throughout the dosing period of 28 days, except those treated with Bipy, with a marked decrease in body weight. The results of the study indicated that Bipy and MPK-TSC had significant adverse effects (P<0.05) on various biochemical indices.

As evidenced by the obtained results, combining MPK-TSC with metal ions resulted in a significant reduction in the toxicity of these compounds.

Lead exposure inflicts severe damage to various body organs. The present study sought to assess the effect of chitosan nanoparticles (NPs) on the prevention of hepatic and renal damage in rats with chronic lead poisoning. The indicators were the levels of oxidative stress and proinflammatory cytokines expression.

We used Rattus norvegicus as the animal model. They were assigned to three groups: negative control, positive control, and treatment (n=8 each). The negative control and treatment groups were the models for chronic lead poisoning, and the serum lead levels were determined by atomic absorption spectrometry. The treatment group was orally administered chitosan NPs at 64 mg/kg for 30 days. The reactive oxygen species (ROS) were measured using 2',7’-dichlorodihydrofluorescein diacetate flow cytometry. The hepatic and renal TNF-α and IL-6 gene expressions were also analyzed.

The mean serum lead level was 0.52 mg/L, validating the rats as the lead poisoning model. The results indicated that the liver and kidneys in the treatment group had the lowest ROS and TNF-α levels compared to those in other groups. The treatment rats had a lower hepatic IL-6 level compared to those in positive controls, although this was higher than that in the negative controls. The renal IL-6 level in the treatment group was the highest among all groups.

As evidenced by the results of this study, chitosan NPs had a protective effect on the liver and kidneys of rats during chronic lead poisoning by reducing the ROS and TNF-α levels; nonetheless, it did not suppress the renal IL-6 expression.

The beetroot extract has long been widely used in the food industry. However, information on its genetic safety is insufficient. In addition, there is evidence to suggest its potential beneficial health effects. The aim of this study was to evaluate the genotoxic and antigenotoxic potentials of red beetroot extract in rats.

The endpoints analyzed were chromosomal aberrations in bone marrow cells and DNA damage in peripheral blood, liver, kidneys, and gastrointestinal tract cells assessed using the alkaline comet assay.

There were no statistically significant differences between the analyzed data from the negative control and those of the groups treated with doses of beetroot extract up to 2000 mg/kg for both of the study endpoints. The findings demonstrated the absence of genotoxicity. The comet assay revealed considerable antigenotoxicity of the beetroot extract (5-100 mg/kg) in the liver, stomach, duodenum, and rectum versus the effects of methyl methanesulfonate and dioxidine mutagens with different mechanisms of action. No anticlastogenic activities were detected in the bone marrow cells while observing the protective effects on blood cells, indicating the tissue specificity for beetroot extract antigenotoxicity.

Based on the study findings, the beetroot extract meets the basic requirements for being a chemopreventive agent. The advantages are low cost, practicality of use, efficacy, and safety. Moreover, this agent may be used to develop food products with chemopreventive properties.

Cancer occurs in 83% of liver diseases. Other risk factors for liver cancer include viral hepatitis, alcohol consumption, industrial chemicals, and a number of toxins. Another major disease that occurs following liver damage is hepatic encephalopathy. This condition arises primarily due to increased blood ammonia levels. Carvacrol, with antioxidant properties, reduces oxidative stress on the liver. The aim of this study was to investigate the effect of carvacrol on the improvement of hepatic encephalopathy in rats.

In this experimental study, 60 male Wistar rats were randomly divided into six groups of 10 each. Liver damage and induction of oxidative stress were caused in the rats by administering thioacetamide (100 mg/kg/day) intraperitoneally for three consecutive days. Carvacrol was administered by gavage at 25, 50, or 100 mg/kg/day after thioacetamide treatment. We investigated the biomarkers of liver damage in the blood, such as alanine transaminase, lactate dehydrogenase, total protein, and bilirubin. We also assessed the effect of oxidative stress, as the key inducer of hepatic encephalopathy, on the liver by measuring the lipid peroxidation, antioxidants, reactive oxygen species, glutathione reserves, and ammonium levels in the serum and brain.

Thioacetamide significantly increased the biochemical markers in the rat sera, reflecting ammonium release and the development of oxidative stress (P<0.05). Conversely, the various doses of carvacrol significantly reduced the levels of biomarkers that are indicative of liver damage (P<0.05).

The study findings provided experimental evidence in favor of the therapeutic effects of carvacrol and against liver injury induced by thioacetamide, leading to encephalopathy.

The kidneys are the main target of lead toxicity as lead is accumulated in and excreted through the kidneys. The main lead toxicity occurs through oxidative stress and lipid peroxidation, causing cellular damage in the kidneys. Moringa leaves contain high levels of flavonoids, with antioxidant effects that are useful in treating diseases accompanied by oxidative stress due to toxicity. Our goal was to analyze the attenuation effects of Moringa leaves extract on lead-induced nephrotoxicity in male Wistar rats.

This research was conducted based on an experimental design and post-tests. Forty-eight Wistar rats were randomly divided into four groups as follows: control group (K), which was given lead acetate at 750 mg/kg/day for 7 days, and three other groups of P1, P2 and P3, which were given lead acetate at the same dose for 7 days followed by administering with the ethanolic extract of Moringa leaves at 1,000, 1,500, and 2,000 mg/kg/day doses orally for 14 days, respectively.

There were improvements in oxidative stress in the kidneys of the study rats, marked by an increase in the serum levels of GSH, GPx, CAT, and SOD, and a decrease in the kidney MDA levels. Kidney disorders can be improved by administering ethanol extract from Moringa leaves, which is characterized by a significant decrease in blood BUN and creatinine levels.

All doses of the ethanolic extract of Moringa leaves reduced the oxidative stress and improved the kidney function impaired due to acute exposure to lead in male Wistar rats.

Silymarin is utilized in the treatment of liver conditions primarily because of its antioxidant properties and its ability to lower blood lipid levels. Propofol, an anesthetic and antioxidant, is harmful to patients with hyperlipidemia. The aim of this study was to investigate the beneficial effects of silymarin and propofol on liver enzymes and blood indices. We also studied the impacts of propofol and silymarin on propofol-induced hyperlipidemia in male Wistar rats.

The rats were divided into four groups: 1) controls; 2) silymarin; 3) propofol; and, 4) combined propofol and silymarin. On the 22nd day after the treatments, all rats were anesthetized, and their blood samples were collected to estimate the levels of AST, ALT, ALP, LDH, TG, TC, LDL-C, and HDL-C. After being sacrificed, the liver was removed from each rat to determine the levels of MDA, GPx, GSH, and CAT. Moreover, histopathological examinations were performed on all liver samples.

Silymarin and propofol, used either separately or in combination, had a favorable effect on the indicators of oxidative stress and the liver’s antioxidant markers. The propofol treatment alone significantly increased the blood lipid parameters. The administration of Silymarin had a modulating effect on propofol-induced hyperlipidemia in rats.

Propofol and silymarin had favorable effects on the liver; however, propofol increased the blood lipids due to its lipid structure, which is a warning for patients with hyperlipidemia. In this regard, silymarin may be considered a protective option, making it a potential treatment for patients experiencing hyperlipidemia induced by propofol.

Breast cancer accounts for 23% of all neoplasias in women, which significantly impacts their physical, mental, and social aspects of life. This study investigated the effect of 8-week aerobic exercise alone or with ferulic acid administration combined with or without zinc oxide on the prevention of breast cancer in a rat model.

A total of 27 rats were randomly divided into 9 groups of 3 rats each as follows: 1) Exercise only; 2) Exercise + ferulic acid; 3) Exercise + zinc; 4) Exercise + ferulic + zinc; 5) Ferulic acid only; 6 ) Zinc; 7) Ferulic + zinc; 8) Positive controls; and 9) Negative controls. In the first week, the aerobic exercise protocol consisted of a 10-minute warm-up period at a speed of 10 m/min for 20 min, which increased to a speed of 18 m/min for 30 min. The ferulic acid supplement was administered to rats intraperitoneally using insulin syringes with a volume of 200 µL. After the last training session, the rats’ breast tissue samples were excised, and the expression levels of BCL2, Bax, and caspase-3 were measured by the real-time polymerase chain reaction method. The data were analyzed by one-way ANOVA and Tukey’s post hoc test (P≥0.05).

The findings showed that intermittent exercise plus ferulic acid-zinc supplementation decreased the BCL2 level in the breast cancer group (P=0.004). Intermittent training supplemented with ferulic acid-zinc increased Bax and caspase-3 levels in the breast cancer group (P=0.001).

Aerobic exercise combined with ferulic acid and zinc nanoparticles inhibited cell apoptosis promoted by breast cancer in rats.