Rapid urbanization and industrialization have led to alarming cadmium (Cd) pollution. Cd is a toxic heavy metal without any known physiological function in the organism, leading to severe health threat to the population. Cd has a long half-life (10–30 years) and thus it represents serious concern as it to a great extent accumulates in organs or organelles where it often causes irreversible damage. Moreover, Cd contamination might further lead to certain carcinogenic and non-carcinogenic health risks. Therefore, its negative effect on population health has to be minimalized. As Cd is able to enter the body through the air, water, soil, and food chain one possible way to defend and eliminate Cd toxicities is via dietary supplements that aim to eliminate the adverse effects of Cd to the organism. Naturally occurring bioactive compounds in food or medicinal plants with beneficial, mostly antioxidant, anti-inflammatory, anti-aging, or anti-tumorigenesis impact on the organism, have been described to mitigate the negative effect of various contaminants and pollutants, including Cd. This study summarizes the curative effect of recently studied bioactive substances and mineral elements capable to alleviate the negative impact of Cd on various model systems, supposing that not only the Cd-derived health threat can be reduced, but also prevention and control of Cd toxicity and elimination of Cd contamination can be achieved in the future.

Cadmium has no known physiological function in the body; however, its adverse effects are associated with cancer and many types of organ system damage. Although much has been shown about Cd toxicity, the underlying mechanisms of its responses to the organism remain unclear. In this study, the role of Tor1, a catalytic subunit of the target of rapamycin complex 2 (TORC2), in Cd-mediated effects on cell proliferation, the antioxidant system, morphology, and ionome balance was investigated in the eukaryotic model organism Schizosaccharomyces pombe. Surprisingly, spectrophotometric and biochemical analyses revealed that the growth rate conditions and antioxidant defense mechanisms are considerably better in cells lacking the Tor1 signaling. The malondialdehyde (MDA) content of Tor1-deficient cells upon Cd treatment represents approximately half of the wild-type content. The microscopic determination of the cell morphological parameters indicates the role for Tor1 in cell shape maintenance. The ion content, determined by inductively coupled plasma optical emission spectroscopy (ICP-OES), showed that the Cd uptake potency was markedly lower in Tor1-depleted compared to wild-type cells. Conclusively, we show that the cadmium-mediated cell impairments in the fission yeast significantly depend on the Tor1 signaling. Additionally, the data presented here suggest the yet-undefined role of Tor1 in the transport of ions.

Stress caused by challenging environmental conditions is often associated with the rapid production of reactive oxygen species (ROS) that dramatically alter cellular redox homeostasis. ROS generation is tightly connected with its utilization, as impaired equilibrium of these processes results in oxidative stress having profound consequences for cell physiology. The balanced action of both antioxidant enzymes and non-enzymatic antioxidants counterbalances the harmful effects of ROS. Despite the functional antioxidant system of the cell, excessive ROS leads to disruption of vital cellular processes which is associated with the development of various lifestyle diseases, mainly cardiovascular diseases, and cancer. Enhanced consumption of foodstuffs with high and balanced antioxidant bioactive compounds is linked with the positive effects of beneficial antioxidants impacting cellular protection resulting in health promotion. In this chapter, we present an outline of how bioactive compounds determine their health-promoting properties.

Acrylamide (AA), is a chemical with multiple industrial applications, however, it can be found in foods that are rich in carbohydrates. Due to its genotoxic and cytotoxic effects, AA has been classified as a potential carcinogen. With the use of spectrophotometry, ICP-OES, fluorescence spectroscopy, and microscopy cell growth, metabolic activity, apoptosis, ROS production, MDA formation, CAT and SOD activity, ionome balance, and chromosome segregation were determined in Schizosaccharomyces pombe. AA caused growth and metabolic activity retardation, enhanced ROS and MDA production, and modulated antioxidant enzyme activity. This led to damage to the cell homeostasis due to ionome balance disruption. Moreover, AA-induced oxidative stress caused alterations in the cell cycle regulation resulting in chromosome segregation errors, as 4.07% of cells displayed sister chromatid non-disjunction during mitosis. Ascorbic acid (AsA, Vitamin C), a strong natural antioxidant, was used to alleviate the negative impact of AA. Cell pre-treatment with AsA significantly improved AA impaired growth, and antioxidant capacity, and supported ionome balance maintenance mainly due to the promotion of calcium uptake. Chromosome missegregation was reduced to 1.79% (44% improvement) by AsA pre-incubation. Results of our multiapproach analyses suggest that AA-induced oxidative stress is the major cause of alteration to cell homeostasis and cell cycle regulation.

Acrylamide (AA) a widely used industrial chemical is also formed during food processing by the Maillard reaction, which makes its exposure to humans almost unavoidable. In this study, we used Schizosaccharomyces pombe as a model organism to investigate AA toxicity (10 or 20 mM concentration) in eukaryotes. In S. pombe, AA delays cell growth causes oxidative stress by enhancement of ROS production and triggers excitement of the antioxidant defence system resulting in the division arrest. Aronia fruit contains a variety of health-promoting substances with considerable antioxidant potential. Therefore, Aronia juice supplementation was tested to evaluate its protective effect against AA-derived perturbations of the organism. Cell treatment with several Aronia juice concentrations ranging from 0 to 2% revealed the best protective effect of 1 or 2% Aronia juice solutions. Both chosen Aronia juice concentrations alleviated AA toxicity through the improvement of the antioxidant cell capacity and metabolic activity by their strong ROS scavenging property. Efficiency of Aronia juice cell protection is dose dependent as the 2% solution led to significantly higher cellular defence compared with 1%. Due to the high similarity of biological processes of S. pombe with higher eukaryotes, the protective effect of Aronia juice against AA toxicity might also apply to higher organisms.

Aluminum (Al), the third most abundant metal in the Earth’s crust, has been preserved for thousands or even millions of years. However, acidic rain and soil acidification, largely driven by human activities related to industrialization and the increased use of Al in daily life, have led to the mobilization of Al from its complex natural resources. This exposure has affected various microorganisms, including bacteria, fungi, protozoa, and yeast, as well as macroorganisms such as plants, animals, and humans, by introducing them to Al in its ionic form. To date, no biological role for Al has been defined in organisms; however, some beneficial effects have been shown, particularly on plant growth. The exposure of living organisms, particularly human cell lines, to chronic and high doses of Al has been the focus of numerous studies. The consequences of such exposure can vary significantly based on the type of organism, their sensitivity, the form of Al, and the dosage used. In plants, these consequences can include inhibited root growth, stunted development, reduced biomass, and disrupted nutrient uptake. In animals, Al exposure can lead to neurological impairments, impaired mineral metabolism, and bone abnormalities. In humans, it may result in encephalopathy, cognitive deficits, microcytic anemia, and an increased risk of Alzheimer’s disease. Unicellular organisms, such as yeast and bacteria, may experience decreased cell viability, inhibited growth, and disrupted metabolic processes. This review discusses the genotoxicity of Al in plants, mammals, and yeast cells, as well as the subsequent detrimental effects on cell cycle and cell proliferation. It also explores the underlying mechanisms and pathways associated with these effects. Furthermore, the types of Al-induced cell death as a response mechanism to Al toxicity and the pathways involved in various cell types were discussed.