Biology subjects

Goldenberg, I.

Publications and source records attributed to Goldenberg, I..

3 recordsLinked to original sources

bioRxiv2025

Low Magnetic Fields Stimulate Cardiac Mitochondrial Bioenergetics with a Bell-Shaped Response: Possibly Via a Radical Pair Mechanism

Studies have shown that low magnetic fields (LMFs) of less than 1 x 10-3 Tesla (T) affect numerous biological events, including bacteria and plant growth, bird migration, and human brain activity. On a cellular level, LMFs affect ion channel activities, intracellular Ca2+ concentrations, and mitochondrial reactive oxygen species (mROS) generation. However, the mechanisms that could account for these effects are controversial. Here, we show that applying a static LMF, ranging from [~]2.7 x 10-4 to [~]1.9 x 10-3 T, to mitochondria isolated from adult rat hearts produced a bell-shaped increase in maximal respiration (Vmax) up to 40%. A similar LMF-induced increase in Vmax was also observed in mitochondria isolated from rat hearts subjected to ischemia-reperfusion (I-R) injury. We then obtained data showing that LMF- mediated bell-shaped response was also observed in the activity of several enzymes involved in oxidative phosphorylation (OXPHOS), including Complexes II, III, and V, and citrate synthase. By contrast, similar LMF caused little change in the enzymatic activity of Complex I. Interestingly, mROS generation responded to LMF with an inverted bell-shaped decrease. We propose a radical pair mechanism of magnetoreception in cytochromes, catalytical reactions, and iron-sulfur clusters within the OXPHOS enzymes to explain how an LMF can increase the likelihood of electron spin transitions from singlet to triplet state and reverse it as the magnetic field strength further increases, resulting in a bell-shaped response. Our results indicate that a narrow range of LMF can enhance mitochondrial bioenergetics and decrease mROS. This may provide a non-invasive approach to treating diseases, such as I-R injury, when energy generation is compromised and oxidative stress is magnified.

biophysics↗

bioRxiv2021

Males perceive honest information from female released sex pheromone in a moth

There is accumulating evidence that male insects advertise their quality to conspecific females through pheromones. However, most studies of female released sex pheromone assume information transfer regarding merely the species of the female and her mating status. We show that more and precise information is conveyed through the female sex pheromone, positioning it as an honest sexual trait. We demonstrate that females in bad physical conditions (small, starved or old) lay significantly fewer eggs than females in good conditions (large, fed or young). The ratio of the sex pheromone blend in gland extracts of female pink bollworm moths accurately describes the female phenotypic condition whereas the pheromone amount in the glands fails to provide an honest signal of quality. Moreover, males use the female released pheromone blend to choose their mates and approach females that signal higher reproductive potential. In addition, surrogating the female effect, using synthetic pheromone blend that represents that of higher quality females (0.6:0.4 ZZ:ZE) more males were attracted to this blend than to the blend representing the population mean (0.5:0.5 ZZ:ZE). Both, female advertisement for males and the male choosiness, suggest that pheromones have evolved as sexual traits under directional, sexual selection.

evolutionary biology↗

bioRxiv2019

A Sex-Specific Switch in Platelet Receptor Signaling Following Myocardial Infarction

BACKGROUNDA Sex-specific, personalized approach to anti-platelet therapy may be important in patients with myocardial infarction (MI).\n\nOBJECTIVESOur goal was to determine whether platelets activate differently in healthy men and women compared to following MI.\n\nMETHODSBlood was obtained from healthy subjects or patients presenting acutely with ST-segment Elevation Myocardial Infarction (STEMI) and non-ST Segment Elevation Myocardial Infarction (NSTEMI). Platelet function through surface receptor activation was examined in healthy subjects, in patients with MI, and in age- and strain-matched mice before and after MI. Multivariate regression analyses revealed clinical variables associated with platelet receptor sensitivity at the time of MI.\n\nRESULTSPlatelets from healthy women are dose-dependently more active compared to men, particularly through the platelet thromboxane signaling pathway (7.8-fold increase in women vs. 3.0-fold in men, P=0.02). At the time of MI, platelet activation through surface protease-activated receptor 1 (PAR1) was less in women than men (3.5-fold vs. 8.5-fold, respectively, P=0.0001). Multivariate regression analyses revealed male sex (P=0.04) and NSTEMI (P=0.003) as independent predictors of enhanced platelet PAR1 signaling at the time of MI. Similar to humans, healthy female mice showed preferential thrombin-mediated platelet activation compared to male mice (8.7-fold vs. 4.8-fold, respectively; P<0.001). In the immediate post-MI environment, male mice showed preferential thrombin-mediated platelet activation compared to female mice (12.4-fold vs. 5.5-fold, respectively; P<0.001).\n\nCONCLUSIONSThese results outline a previously unrecognized sex-dependent platelet phenotype where inhibition of thrombin signaling in the peri-MI environment--particularly in males--may be an important consideration.\n\nCONDENSED ABSTRACTPreclinical studies evaluating anti-platelet drugs are generally conducted in platelets isolated from healthy individuals. Growing evidence suggests changes in platelet signaling properties in certain disease conditions compared to healthy platelets may alter the response to anti-platelet medications. This investigation revealed that platelets from men and women who are healthy and following MI signal differently, particularly through thromboxane and PAR1 receptors. This effect was especially noted in patients with NSTEMI compared to STEMI. These observations raise the possibility of considering a sex-specific anti-platelet regimen for males and females in atheroembolic vascular diseases such as NSTEMI.

molecular biology↗