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Myrtenol is a monoterpene with multiple pharmacological activities. However, although monoterpenes have been proposed to play beneficial roles in a variety of cardiac disorders, pharmacological actions of myrtenol in the heart are not yet reported. Hence, the aim of this study was to evaluate whether myrtenol promotes cardioprotection against myocardial ischemia-reperfusion (IR) injury, and the mechanisms involved in these effects. Male Wistar rats were orally treated for seven consecutive days with myrtenol (50 mg/kg) or N-acetyl cysteine (1.200 mg/kg, NAC). Afterward, hearts were subjected to myocardial IR injury. Here, we show that the severe impairment of contractile performance induced by IR was significantly prevented by myrtenol or NAC. Moreover, myrtenol abolished aberrant electrocardiographic waveform (ST-segment elevation), as well as reduced life-threatening arrhythmias and infarct size induced by IR injury. Importantly, myrtenol fully prevented the massive increase of cardiac reactive oxygen species generation and oxidative stress damage. Accordingly, myrtenol restored the impairment of endogenous antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase and reductase) activities and balance of pro- and anti-apoptotic pathways (Bax and Bcl-2), associated with decreased apoptotic cells. Taken together, our data show that myrtenol promotes cardioprotection against IR injury through attenuation of oxidative stress and inhibition of pro-apoptotic pathway.

Objective: The mechanisms involved in NOX5 activation in atherosclerotic processes are not completely understood.  This study tested the hypothesis that lysophosphatidylcholine (LPC), a proatherogenic component of oxLDL, induces endothelial calcium influx, which drives NOX5-dependent reactive oxygen species (ROS) production, oxidative stress, and endothelial cell dysfunction.  Approach: Human aortic endothelial cells (HAEC) were stimulated with LPC (10-5 M, for different time points).  Pharmacological inhibition of NOX5 (Melittin, 10-7 M) and NOX5 gene silencing (siRNA) were used to determine the role of NOX5-dependent ROS production in endothelial oxidative stress induced by LPC.  ROS production was determined by lucigenin assay and electron paramagnetic spectroscopy (EPR), calcium transients by Fluo4 fluorimetry, and NOX5 activity and protein expression by pharmacological assays and immunoblotting, respectively. Results: LPC increased ROS generation in endothelial cells at short (15 min) and long (4 h) stimulation times.  LPC-induced ROS was abolished by a selective NOX5 inhibitor and by NOX5 siRNA. NOX1/4 dual inhibition and selective NOX1 inhibition only decreased ROS generation at 4 h.  LPC increased HAEC intracellular calcium, important for NOX5 activation, and this was blocked by nifedipine and thapsigargin.  Bapta-AM, selective Ca2+ chelator, prevented LPC-induced ROS production.  NOX5 knockdown decreased LPC-induced ICAM-1 mRNA expression and monocyte adhesion to endothelial cells. Conclusion: These results suggest that NOX5, by mechanisms linked to increased intracellular calcium, is key to early LPC-induced endothelial oxidative stress and pro-inflammatory processes.  Since these are essential events in the formation and progression of atherosclerotic lesions, this study highlights an important role for NOX5 in atherosclerosis.

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Occupational factors can lead to breast cancer, though the relationship between these variables is not well established. The objective of this study was to search the relevant literature for information on the association between breast cancer and exposure to occupational risk factors. For that purpose, electronic databases were searched using the following keywords: breast cancer and occupational exposures. A total of 40 articles published in the 10-year period from 2009 to 2019 were included in this review. Workers exposed to metals such as cadmium, chemical products, radiation and night work were more susceptible to breast cancer. The findings showed significant evidence to support an association between breast cancer and some chemical products, ionizing radiation and night work. However, most studies have difficulty establishing a causal relationship between these variables, pointing to the need for further investigation of these issues.

Background: Occupational risk factors are associated with many types of neoplasms including cervical cancer. Objective: To review the specialized literature for evidence on the relationship between cervical cancer and exposure to occupational hazards. Methods: Literature search in electronic databases using keywords cervical cancer and occupational risk. Results: Workers occupationally exposed to tobacco, fungi or bacteria, metalworking fluids and tetrachloroethylene used in dry cleaning and for metal degreasing exhibited higher susceptibility to cervical cancer. Conclusion: Few studies sought to investigate relationships between cervical cancer and occupational hazards, which hinders the attempts at establishing a causal link.

Resumo Fundamento: A (-)-carvona é um monoterpeno encontrado em óleos essenciais com atividade antioxidante e anti-inflamátoria. Objetivos: O objetivo deste estudo foi analisar a propriedade antiarrítmica da (-)-carvona no coração de rato e seus efeitos sobre a sinalização de Ca +2 intracelular. Métodos: Os efeitos da (-)-carvona foram avaliados sobre a contratilidade atrial (0,01 – 4 mM) e ventricular (0,5 mM), e no eletrocardiograma (0,5mM). A fração de encurtamento, a corrente de cálcio do tipo L (I Ca,L ) e a sinalização de Ca +2 foram medidas no cardiomiócito isolado (0,5 mM). O efeito antiarrítmico foi avaliado no modelo de arritmia induzida por sobrecarga de cálcio (0,5 mM) (n = 5). Um p < 0,05 foi adotado como nível de significância estatística. Resultados: No átrio, a (-)-carvona causou inotropismo negativo de maneira concentração-dependente (EC 50 0,44 ± 0,11 mM) e diminuiu o inotropismo positivo induzido pelo CaCl 2 (0,1 – 8,0 mM) e BAY K8644 (5 - 500 nM), um agonista de canal de cálcio do tipo L. Em coração isolado, a (-)-carvona (0,5mM) reduziu a contratilidade ventricular em 73% e a frequência cardíaca (em 46%), aumentou o Pri (30,7%, tempo desde o início da onda P até a onda R) e o QTc (9,2%, uma medida de despolarização e repolarização dos ventrículos), sem mudar a duração do complexo QRS. A (-)-carvona diminuiu a fração de encurtamento (61%), a (I Ca,L ) (79%) e o transiente intracelular de Ca +2 (38%). Além disso, a (-)-carvona apresentou ação antiarrítmica, identificada pela redução do escore de arritmia (85%) e ocorrência de fibrilação ventricular. Conclusão: A (-)-carvona reduz a entrada de Ca +2 através de canais de Ca +2 do tipo L e, assim, diminui a contratilidade cardíaca e o Ca +2 intracelular e apresenta promissora atividade antiarrítmica no coração de ratos.