Understanding morphological, biochemical, and functional aspects of cell death is essential for targeting new cancer therapies. Even though many different mechanisms of cell death are identified, it is crucial to highlight the role of new and lesser-known pathways, including methuosis, alkaliptosis, and oxeiptosis. The aim of this review was to summarize the data about cell death mechanisms—methuosis, alkaliptosis, and oxeiptosis—and their role in cancer treatment. Unique molecular mechanisms and cellular outcomes characterize each of these forms of cell death. This research on methuosis, alkaliptosis, and oxeiptosis provides a better understating of cell death biology and creates novel opportunities for neoplasm management.

Lipid peroxidation (LPO) is a process where polyunsaturated fatty acids (PUFA) in cellular membranes are oxidized. This process is mediated by reactive oxygen species (ROS) and leads to the formation of reactive products, including 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), and oxidized phospholipids. At low concentrations these products act as second messengers in adaptive redox signalling and metabolic homeostasis, whereas at higher concentrations they compromise membrane integrity and promote cell death. Lipid peroxidation plays a crucial role in anticancer therapies. Here we focus on three mechanistically complementary drugs—sorafenib, cisplatin, and olaparib—because each converges, directly or indirectly, on the redox/LPO axis (system xc−/GPX4 modulation, mitochondrial ROS, and SLC7A11 regulation, respectively), modulating tumor cell responses by inducing PUFA oxidation, mitochondrial dysfunction, and membrane damage. However, tumor cells have several protective pathways against oxidative stress, such as increased expression of glutathione peroxidase 4 (GPX4), the SLC7A11 system Xc, and detoxification of reactive aldehydes. Enrichment of membranes with PUFA increases susceptibility to lipid peroxidation and ferroptosis, thereby sensitizing tumor cells to therapy, whereas enrichment with monounsaturated fatty acids (MUFA), driven by the SREBP1–SCD1 axis, limits peroxidation and confers resistance. Among regulated cell death modalities, ferroptosis is strictly dependent on lipid peroxidation, whereas apoptosis, necrosis, necroptosis, pyroptosis, and immunogenic cell death can be modulated by lipid peroxidation but do not universally require it. Collectively, these mechanisms indicate that lipid peroxidation is an important—though not exclusive—determinant of anticancer drug sensitivity and resistance, and that its dual, context-dependent role (tumor-suppressive at high flux, tumor-promoting under chronic, sub-lethal exposure) must be considered when designing LPO-based therapeutic strategies.

Background/Objectives: Thyroid hormones, considered safe in therapeutic doses, are used to treat hypothyroidism, a common condition. Due to a combination of factors, including their mechanism of action, availability, and low price, these drugs are used illegally, mainly to improve performance, to assist in weight loss, or for attempting suicide. Their overuse can lead to serious health consequences, including death. Although thyroid hormones are abused, there are no studies assessing the scale, characteristics, and consequences of their illegal use. The aim of this study was to evaluate case reports of thyroid hormone poisoning from the last 30 years, assessing their dynamics and characteristics. Methods: Full-text clinical case studies were obtained by searching PubMed, Google Scholar, MEDLINE, Embase, Web of Science, and Scopus for the following terms: “thyroid hormones”, “thyroxine”, “levothyroxine”, “triiodothyronine”, and “liothyronine”, as well as “intoxication”, “overdose”, and “poisoning”. This study adhered to Preferred Reporting for Systematic Reviews and Meta-analyses (PRISMA) guidelines for systematic reviews. Results: Thyroid hormones are abused particularly by athletes, persons trying to lose weight, or those attempting suicide. There has been an upward trend in thyroid hormone poisoning over the past 30 years, particularly since 2015. The same trend has been observed in cases of thyroid hormone use for doping, among other performance-enhancing drugs. Thyroid hormone use for doping was the most common cause of poisoning with these drugs, with other clinical manifestations from poisonings due to other causes. No upward trend has been observed in the use of thyroid hormones in suicide attempts since 2017, as this number remains stable. Conclusions: Although exploratory in nature, our work indicates that thyroid hormone poisoning, associated mostly with the illegal use of anabolic–androgenic steroids, exhibits an increasing tendency. Moreover, thyroid hormone abuse is an important issue in suicidology.

Introduction. This study aimed to determine changes in the level of alpha-amylase and cortisol in the saliva of male and female basketball players after one session of basketball training. Additionally, the study examined whether differences existed between females and males in the levels of these biomarkers in response to physical exertion. Material and Methods. The study involved 30 athletes from academic leagues (17 females and 13 males). The training session consisted of warm-up, conditioning, and tactical drills and lasted for 90 minutes. A sample of saliva was obtained before and after the training session. Salivary flow, alpha-amylase, and cortisol were measured. Wilcoxon Signed-Rank and U-Mann were used for statistical analysis at a significance level of 0.05. Results. After the training session, a significant increase in salivary cortisol levels was observed in females (p < .05), whereas in males, a significant increase (p < .05) was noted in salivary alpha-amylase levels. There were no significant differences in alpha-amylase and cortisol levels between females and males before and after exercise. Conclusions. These results suggest that the response to physical exertion may vary depending on gender, which highlights a need for further research targeting the relationship between exercise intensity, hormonal response, and body adaptation.