The drugs used to treat cancer not only kill fast-growing cancer cells, but also kill or slow the growth of healthy cells, causing systemic toxicities that lead to altered functioning of normal cells. Most chemotherapeutic agents have serious toxicities associated with their use, necessitating extreme caution and attention. There is a growing interest in herbal remedies because of their pharmacological activities, minimal side effects, and low cost. Thymoquinone, a major component of the volatile oil of Nigella sativa Linn, also known as black cumin or black seeds, is commonly used in Middle Eastern countries as a condiment. It is also utilized for medicinal purposes and possesses antidiabetic, anti-cancer, anti-inflammatory, hepatoprotective, anti-microbial, immunomodulatory, and antioxidant properties. This review attempts to compile the published literature demonstrating thymoquinone’s protective effect against chemotherapeutic drug-induced toxicities.

Multiple prescriptions for different medications may be needed for chronic conditions, increasing the risk of polypharmacy. The WHO defined polypharmacy as “the administration of many drugs at the same time or the administration of an excessive number of drugs”. The primary goal of this study was to evaluate polypharmacy in patients with chronic liver disease and to identify potential drug-drug interactions associated with it. A cross-sectional study was conducted at a tertiary care hospital in Mangalore, Karnataka, for six months, from November 2020 to April 2021. The study involved 118 patients with chronic liver disease from various age groups. Data was gathered by analyzing patients' medical records kept on the ward and interviewing them individually. In admission and discharge prescriptions, polypharmacy was examined. Online interaction checkers from Drugs.com and Medscape were used to interpret potential drug-drug interactions. The SF-36 and Chronic Liver Disease Questionnaire were used to measure the quality of life. The data obtained were analyzed statistically to determine the significant correlation. The number of prescribed drugs was significantly correlated (P = 0.018) with the severity of liver disease in Child-Pugh categories B and C. Additionally, moderate polypharmacy reduced quality of life (P < 0.05), and the physical health category was significantly associated with disease severity (P < 0.05). Drug-drug interactions were found in 108 out of the 118 examined prescriptions, totaling 586 interactions in the admission list and 405 interactions in the discharge list. If the potentially serious main drug interaction identified in this study is not well monitored, it could lead to a serious, potentially fatal health condition. Despite being advised, safety is not always guaranteed by liver enzyme monitoring. Therefore, healthcare providers must take additional precautions to avoid inappropriate prescribing, minimize side effects, and ensure drug safety.

5-Fluorouracil (5-FU) is widely used in chemotherapy but poses serious risks of cardiotoxicity, which can significantly affect treatment outcomes. Identifying interventions that can prevent these adverse effects without undermining anticancer efficacy is crucial. This study investigates the efficacy of Thymoquinone (TQ) and Hesperidin (HESP) in preventing cardiotoxicity induced by 5-FU in Wistar rats and elucidates the molecular interactions through docking studies. We employed an experimental design involving multiple groups of Wistar rats exposed to 5-FU, with and without the concurrent administration of TQ and HESP. Cardiac function markers, oxidative stress indicators, and inflammatory markers were assessed. Additionally, molecular docking was used to analyze the interaction of TQ and HESP with key inflammatory proteins. Treatment with TQ and HESP not only lowered levels of cardiac enzymes but also improved antioxidant capacity and reduced inflammation in cardiac tissues. Notably, the combination of TQ and HESP provided more significant protective effects than either agent alone. Molecular docking supported these findings, showing effective binding of TQ and HESP to inflammatory targets. TQ and HESP demonstrate potential as protective agents against cardiotoxicity in 5-FU-treated rats, with their combined use offering enhanced protection. These findings suggest a viable strategy for reducing cardiac risks associated with 5-FU chemotherapy.

Anticancer medications often lead to organ toxicity, affecting patients’ quality of life. Phytochemical compounds like Thymoquinone (TQ) and Hesperidin (HESP) have shown promise in mitigating anticancer drug-induced toxicity. However, their ability to protect against nephrotoxicity produced by 5- Fluorouracil (5-FU) remains unexplored. To assess the protective efficacy of TQ, HESP, and their combination against nephrotoxicity induced by 5-FU in both in vitro and in vivo settings. Human Embryonic Kidney (HEK293) cells were subjected to various concentrations of 5-FU, TQ, and HESP, with cell viability assessed using the MTT assay. Apoptosis was evaluated through Acridine orange-Ethidium bromide dual staining (AO- EB). In vivo experiments utilized male Wistar albino rats, which received treatments of 5-FU alone, in combination with TQ, HESP, and both. Subsequent biochemical and histological analyses were conducted on serum and kidney tissue samples. In vitro studies revealed dose- dependent cytotoxicity of 5-FU, while TQ and HESP showed minimal toxicity. Combination treatment significantly improved cell viability compared to 5-FU alone. In vivo studies indicated that the administration of 5-FU resulted in elevated levels of serum creatinine and blood urea nitrogen (BUN), suggestive of kidney dysfunction, which were attenuated by TQ, HESP, or their combination. TQ and HESP also restored antioxidant enzyme activity and reduced inflammatory markers in kidney tissues. Histological analysis showed significant protection against 5-FU- induced renal damage with combination therapy. Our findings suggest that TQ and HESP, alone or in combination, possess protective effects against 5-FU-induced nephrotoxicity, possibly through antioxidant and anti-inflammatory mechanisms. These results highlight the potential of herbal medicines as adjunctive therapies to mitigate chemotherapy-induced organ toxicity and improve patient outcomes. Additional investigation is necessary to clarify the fundamental molecular mechanisms involved and to corroborate these findings in clinical contexts.

Background Polypharmacy, or taking multiple medications simultaneously, is a common occurrence in the elderly population, increasing the risk of adverse drug reactions (ADRs) and drug-drug interactions (DDIs) requiring the intricate management of multiple comorbid conditions. Pharmacogenomics, the study of genetic differences affecting drug metabolism and response, can offer hope of more tailored medication regimens and enhanced therapeutic response. Aim The aim of this study is to create pharmacogenomic profiles of elderly patients in order to determine patient-specific genetic variation contributing to drug response, ultimately influencing the efficacy of drug therapy and increasing the potential risk of ADRs. Method A cross-sectional study was conducted involving 50 geriatric patients aged 60 years or older receiving multi-drug therapy. Saliva samples were collected and genotyped using the Infinium™ Global Screening Array v3.0 BeadChip. Single nucleotide polymorphisms (SNPs) associated with drug response were identified using the PharmGKB database. SNPs with significant clinical relevance were analysed, and pharmacogenomic profiles were visualized to assess risks for ADRs and altered drug efficacy. Results Out of 1,243 SNPs analysed per individual, 561 SNPs with two risk alleles were identified. Fifteen SNPs were present in over 90% of participants, with significant variants observed in genes such as CYP2C9 (associated with warfarin metabolism), TPMT (linked to methotrexate dosing), and SLCO1B3 (associated with docetaxel toxicity). More than 50% of participants had two or more risk alleles, highlighting their predisposition to ADRs and altered drug metabolism. Conclusion The findings of this study emphasize the transformative potential of pharmacogenomics for rationalizing drug therapy among elderly patients, especially when they are susceptible to polypharmacy. Through identification of major genetic differences such as CYP2C9, TPMT and other pharmacogenes the study underlines the requirement for individualized pharmacotherapy based on distinct genetic profiles.