To contribute new information to the pyrethroid pesticide α-cypermethrin toxicity profile, we evaluated its effects after oral administration to Wistar rats at daily doses of 2.186, 0.015, 0.157, and 0.786 mg/kg bw for 28 days. Evaluations were performed using markers of oxidative stress, cholinesterase (ChE) activities, and levels of primary DNA damage in plasma/whole blood and liver, kidney, and brain tissue. Consecutive exposure to α-cypermethrin affected the kidney, liver, and brain weight of rats. A significant increase in concentration of the thiobarbituric acid reactive species was observed in the brain, accompanied by a significant increase in glutathione peroxidase (GPx) activity. An increase in GPx activity was also observed in the liver of all α-cypermethrin-treated groups, while GPx activity in the blood was significantly lower than in controls. A decrease in ChE activities was observed in the kidney and liver. Treatment with α-cypermethrin induced DNA damage in the studied cell types at almost all of the applied doses, indicating the highest susceptibility in the brain. The present study showed that, even at very low doses, exposure to α-cypermethrin exerts genotoxic effects and sets in motion the antioxidative mechanisms of cell defense, indicating the potential hazards posed by this insecticide.

The objective of this study was to evaluate the influence of high-fat (HF) and cafeteria diet (CAF) diets and sex on the metabolism of important fatty acids in the liver and perirenal fat tissue. Dietary treatments induced changes in the fatty acid profile in comparison to the untreated group, but the characteristic differences between treated groups were also observable. The HF diet induced an increase in the content of C16:1n-7 and C18:1n-7 in the liver phospholipids (PL) and triglycerides (TG) and perirenal fat tissue compared to the control and CAF diet. The CAF diet induced a more drastic decrease in both n-3 and n-6 polyunsaturated fatty acids (PUFA), including depletion of eicosapentaenoic acid (EPA). The CAF diet also increased the content of n-6 docosapentaenoic acid (DPAn-6) in the liver and decreased it in the perirenal fat. Sex also had a significant influence on the fatty acid profile, but the variables with the highest differences between the CAF and HF treatments were identical in the male and female rats. In this study, we have established that two dietary models of non-alcoholic fatty liver disease (NAFLD) led to characteristic changes in the hepatic and perirenal fat fatty acid profile, in contrast to the control diet and in comparison with each other. These differences could play an important role in the interpretation of the experimental results of nutritional studies.

Currently we are faced with an ever-growing use of Δ⁹-tetrahydrocannabinol (THC) preparations, often used as supportive therapies for various malignancies and neurological disorders. As some of illegally distributed forms of such preparations, like cannabis oils and butane hash oil, might contain over 80% of THC, their consumers can become intoxicated or experience various detrimental effects. This fact motivated us for the assessments of THC toxicity in vivo on a Wistar rat model, at a daily oral dose of 7 mg/kg which is comparable to those found in illicit preparations. The main objective of the present study was to establish the magnitude and dynamics of DNA breakage associated with THC exposure in white blood and brain cells of treated rats using the alkaline comet assay. The extent of oxidative stress after acute 24 h exposure to THC was also determined as well as changes in activities of plasma and brain cholinesterases (ChE) in THC-treated and control rats. The DNA of brain cells was more prone to breakage after THC treatment compared to DNA in white blood cells. Even though DNA damage quantified by the alkaline comet assay is subject to repair, its elevated level detected in the brain cells of THC-treated rats was reason for concern. Since neurons do not proliferate, increased levels of DNA damage present threats to these cells in terms of both viability and genome stability, while inefficient DNA repair might lead to their progressive loss. The present study contributes to existing knowledge with evidence that acute exposure to a high THC dose led to low-level DNA damage in white blood cells and brain cells of rats and induced oxidative stress in brain, but did not disturb ChE activities.

Heavy metals are dangerous systemic toxicants that can induce multiple organ damage, primarily by inducing oxidative stress and mitochondrial damage. Clinoptilolite is a highly porous natural mineral with a magnificent capacity to eliminate metals from living organisms, mainly by ion-exchange and adsorption, thus providing detoxifying, antioxidant and anti-inflammatory medicinal effects. The in vivo efficiency and safety of the oral administration of clinoptilolite in its activated forms, tribomechanically activated zeolite (TMAZ) and Panaceo-Micro-Activated (PMA) zeolite, as well as the impact on the metallic biodistribution, was examined in healthy female rats. Concentration profiles of Al, As, Cd, Co, Pb, Ni and Sr were measured in rat blood, serum, femur, liver, kidney, small and large intestine, and brain using inductively coupled plasma mass spectrometry (ICP-MS) after a 12-week administration period. Our results point to a beneficial effect of clinoptilolite materials on the concentration profile of metals in female rats supplemented with the corresponding natural clinoptilolite materials, TMAZ and PMA zeolite. The observed decrease of measured toxicants in the kidney, femur, and small and large intestine after three months of oral intake occurred concomitantly with their most likely transient release into the bloodstream (serum) indicative of a detoxification process.

There is growing interest regarding the use of herbal preparations based on Cannabis sativa for medicinal purposes, despite the poorly understood interactions of their main constituent Δ⁹-tetrahydrocannabinol (THC) with conventional drugs, especially cytostatics. The objective of this pilot study was to prove whether the concomitant intake of THC impaired liver function in male Wistar rats treated with the anticancer drug irinotecan (IRI), and evaluate the toxic effects associated with this exposure. IRI was administered once intraperitoneally (at 100 mg/kg of the body weight (b.w.)), while THC was administered per os repeatedly for 1, 3, and 7 days (at 7 mg/kg b.w.). Functional liver impairments were studied using biochemical markers of liver function (aspartate aminotransferase—AST, alanine aminotransferase—ALP, alkaline phosphatase—AP, and bilirubin) in rats given a combined treatment, single IRI, single THC, and control groups. Using common oxidative stress biomarkers, along with measurement of primary DNA damage in hepatocytes, the degree of impairments caused at the cellular level was also evaluated. THC caused a time-dependent enhancement of acute toxicity in IRI-treated rats, which was confirmed by body and liver weight reduction. Although single THC affected ALP and AP levels more than single IRI, the levels of liver function markers measured after the administration of a combined treatment mostly did not significantly differ from control. Combined exposure led to increased oxidative stress responses in 3- and 7-day treatments, compared to single IRI. Single IRI caused the highest DNA damage at all timepoints. Continuous 7-day oral exposure to single THC caused an increased mean value of comet tail length compared to its shorter treatments. Concomitant intake of THC slightly affected the levels of IRI genotoxicity at all timepoints, but not in a consistent manner. Further studies are needed to prove our preliminary observations, clarify the underlying mechanisms behind IRI and THC interactions, and unambiguously confirm or reject the assumptions made herein.

Zinc is an essential micronutrient involved in structural, catalytic, and regulatory functions across all levels of biological organization. Despite substantial advances over the past two decades, the zinc literature remains highly fragmented, with mechanistic, nutritional, and clinical findings often reported in isolation. Additionally, the synergistic interactions between zinc and other micronutrients—particularly minerals and vitamins—are dispersed across multiple research domains, complicating efforts to understand their integrated roles in maintaining homeostasis. Recent developments in artificial intelligence (AI) present new opportunities to consolidate these data, enabling multi-scale analyses of zinc-dependent processes and the broader zinc interactome. Although a complete map of the zinc interactome is not yet feasible, an integrative perspective is needed to contextualize zinc’s contributions within the framework of the hallmarks of health. This narrative review highlights zinc’s involvement in cellular maintenance, metabolic regulation, stress response, and systemic physiological function. It further examines how disruptions in zinc status, alone or in combination with other nutrient imbalances, contribute to clinically relevant disorders. By combining current knowledge across molecular, cellular, and systems biology levels, this review illustrates zinc’s pleiotropic effects on physiological resilience and healthspan, with particular emphasis on its role in nutritional status, homeostatic regulation, and overall human health.