Dimethyl sulphoxide is extensively used in chemical, pharmaceutical and biomedical applications, but its specific biological actions remain largely elusive. The aim of this study was to comprehensively explore the effects of dimethyl sulphoxide on eukaryotic growth and senescence by using the budding yeast Saccharomyces cerevisiae as a reliable model organism. Rather than focusing on single cells or on either the replicative or the chronological lifespan approach, well-established microbiological procedures were integrated to monitor a combination of physiological parameters. Cell proliferation, survival, reproductive competence and morphology were recorded at various time points during incubation of asynchronous yeast populations with increasing concentrations of dimethyl sulphoxide. The findings demonstrated a dose-dependent inhibitory effect of the compound on yeast proliferation, survival and reproduction. In parallel, dimethyl sulphoxide induced the acquisition of the non-revertible petite phenotype and promoted morphological alterations that characterize senescence, driving the yeast populations towards the reproductive incompetent state. These findings point to the need for the investigation of the complex cellular and/or molecular mechanisms underlying the actions of dimethyl sulphoxide in eukaryotic cells and for the evaluation of their exploitation potential.

<b><i>Background:</i></b> Non-steroidal anti-inflammatory drugs (NSAIDs) represent one of the most prevalent causes of drug hypersensitivity reactions (DHRs), yet the underlying processes are far from clear. Despite the established role of histamine in allergic reactions, its precise implication in DHRs is elusive. <b><i>Objectives:</i></b> This study aimed to explore the connection of basal blood histamine levels to the reported NSAID hypersensitivity. <b><i>Methods:</i></b> Sixteen patients reporting hypersensitivity reactions to a single or multiple NSAIDs and/or paracetamol and 18 healthy volunteers serving as the normal control group enrolled in the study. The medical history was recorded and histamine was quantified spectrophotofluorometrically in whole peripheral blood and plasma. <b><i>Results:</i></b> Compared to the normal group, plasma but not whole blood histamine levels were significantly higher in patients (<i>p</i> &#x3c; 0.001), mainly in the subgroup reporting hypersensitivity to a single agent (<i>p</i> &#x3c; 0.001). Plasma histamine levels were significantly correlated with the culprit drug selectivity for cyclooxygenase (COX) isozymes (<i>p</i> &#x3c; 0.001), with higher levels being obtained in patients reporting reactions to COX-1 than to COX-2 selective inhibitors (<i>p</i> &#x3c; 0.05). <b><i>Conclusions:</i></b> The findings provide first evidence connecting basal blood histamine levels to the reported NSAID-triggered DHRs. Prospective studies are expected to decipher the contribution of histamine-associated parameters to the mechanisms underlying DHRs.

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Background: Drug hypersensitivity reactions (DHRs; drug allergy) affect >7% of the population and comprise 15% of adverse drug reactions. Being potentially life threatening and a frequent cause of post-marketing drug withdrawal, DHRs represent important public health and medical concerns. Non-steroidal anti-inflammatory drugs (NSAIDs) are only second to antibiotics as the most frequent DHR-inducing agents. However, solid knowledge on the underlying mechanisms is virtually lacking. Non-standardized studies and DHR misdiagnosis repeatedly lead to misconceptions and to the use of more-expensive and potentially less-effective drugs. This study aimed at critically evaluating a DHR database in an effort to dissect reliable and useful information on NSAID-induced DHRs. Methods: A proprietary database of DHRs reported in the Outpatient Allergy