Oxidative and osmotolerant effects in Salvator merianae (Squamata: Teiidae) red blood cells during hibernation

Hibernation is a natural condition of animals that lives in the temperate zone, although some tropical lizards also experience hibernation annually, such as the lizard native from South America, Salvator merianae, or “tegu” lizard. Even though physiological and metabolic characteristic associated with hibernation have been extensively studied, possible alterations in the red blood cells (RBC) integrity during this period remains unclear. Dehydration and fasting are natural consequences of hibernating for several months and it could be related to some cellular modifications. In this study, we investigated if the osmotic tolerance of RBCs of tegu lizard under hibernation is different from the cells obtained from animals while normal activity. Additionally, we indirectly investigated if the RBCs membrane of hibernating tegus could be associated with oxidation by quantifying oxidized biomolecules and the activity of antioxidant enzymes. Our findings suggest that RBCs are more fragile during the hibernation period, although we did not find evidence of an oxidative stress scenario associated with the accentuated fragility. Even though we did not exclude the possibility of oxidative damage during hibernation, we suggested that an increased RBCs volume as a consequence of hypoosmotic blood during hibernation could also affect RBCs integrity as noted.

Human Cytomegalovirus Egress: Overcoming Barriers and Co-Opting Cellular Functions

The assembly of human cytomegalovirus (HCMV) and other herpesviruses includes both nuclear and cytoplasmic phases. During the prolonged replication cycle of HCMV, the cell undergoes remarkable changes in cellular architecture that include marked increases in nuclear size and structure as well as the reorganization of membranes in cytoplasm. Similarly, significant changes occur in cellular metabolism, protein trafficking, and cellular homeostatic functions. These cellular modifications are considered integral in the efficient assembly of infectious progeny in productively infected cells. Nuclear egress of HCMV nucleocapsids is thought to follow a pathway similar to that proposed for other members of the herpesvirus family. During this process, viral nucleocapsids must overcome structural barriers in the nucleus that limit transit and, ultimately, their delivery to the cytoplasm for final assembly of progeny virions. HCMV, similar to other herpesviruses, encodes viral functions that co-opt cellular functions to overcome these barriers and to bridge the bilaminar nuclear membrane. In this brief review, we will highlight some of the mechanisms that define our current understanding of HCMV egress, relying heavily on the current understanding of egress of the more well-studied α-herpesviruses, HSV-1 and PRV.

Keratinocyte cellular damage induced by pesticide doses below the cytotoxic level evidenced by electrical impedance and broadband dielectric spectroscopy

Cellular response of a normal human keratinocyte cell line exposed to non-cytotoxic doses of a deltamethrin-based pesticide was investigated by means of two different electrical impedance data spectroscopy approaches: Nyquist plot and broadband dielectric spectroscopy. The measurements have shown that the membrane capacity increases with pesticide concentration and this facilitates the electric current through cell membranes. Furthermore, the impedance of the extracellular matrix also increases with pesticide concentration, thus reducing the electric current outside the cell. Dielectric permittivity changes in the cellular samples at frequency larger than 100 Hz. Fluorescence measurements emphasized an increase of neutral membrane lipids as consequence of the pesticide exposure. Comparison of fluorescence response of pesticide exposed cells with the control ones showed a time increase of the emission intensity, suggesting the existence of a membrane lipid response aimed at repairing of the cell damage due to pesticide exposure. Therefore, both the spectroscopic techniques have demonstrated to be potential means to investigate the response to cell stress and damage. This opens up new possibilities in the early diagnosis of cellular modifications related to pesticides exposure of cells.

Cellular Changes in Buccal Mucosa from Farmers Exposed to Glyphosate / Alterações Celulares na Mucosa Bucal de Agricultores Expostos ao Glifosato

This study evaluated the sociodemographic characteristics and behavior of the oral mucosa epithelium exposured to the herbicide glyphosate of family farmers in Cerro Largo, RS, Brazil. 120 individuals were selected for social data collection through interviews. According to the results, most of the interviewees uses glyphosate between 5-10 years, being exposed between 30 minutes to one hour each application and applying the herbicide 1-2 times a year. After the interview, we selected the subjects to the Micronucleus (MN) test. For this test, oral smears were performed in three distinct regions (cheek, mouth floor and tongue edges) of 10 test subjects (exposed to glyphosate, non-smoker and non-alcoholic) and 10 control subjects. Results showed that glyphosate exposure increased the frequency of MN in the test group (p = 0.0002), as well as the frequency of other cellular alterations, such as brokenegg (p = 0.001), binucleation (p = 0.0001) and karyolysis (p = 0.0004). Based on these findings, the extent use of glyphosate may be causing damage to the oral mucosa epithelium and this might respond adaptively through cellular modifications.

Evaluation of cerebroprotective effect of Ricinus communis leaves against ischemia reperfusion injury in rats

Background Ricinus communis (RC) has been used for a long time as natural origin medicine in the treatment of central nervous system ailments. This present study was designed to identify the possible role of Ricinus communis leaves extract against ischemia-reperfusion induced-neurobehavioral changes, oxidative stress, histopathological and cellular modifications in the brain. Methods Sprague Dawley (SD) rats (200–250 g) were induced to bilateral common carotid artery occlusion (BCCAO) for around 30 min later subjected to reperfusion for 24 h to induce cerebral injury by reperfusion. Ricinus communis leaves extract (250 and 500 mg/kg, p.o) was administered continuously for 14 days and on the 15th-day animals were subjected to ischemia-reperfusion injury. Different behavioral tests and biochemical parameters were assessed subsequently. Results Fourteen days Ricinus communis leaves extract (250 and 500 mg/kg, p.o.) treatment very significantly improved neurobehavioral alterations when compared to control ischemia-reperfusion. Ricinus communis leaves extract (250 and 500 mg/kg, p.o.) kg, i.p. treatment significantly attenuated oxidative damage when compared to ischemia-reperfusion (I/R) group animals. In addition, Ricinus communis leaves extract treatment was well supported histopathologically when compared to the ischemia-reperfusion (I/R) group. Conclusion The data from this study recommend that treatment with Ricinus communis leaves extract increases the antioxidant protection against BCCAO-induced global cerebral ischemia and demonstrates neuroprotective activity.

Age-associated changes to neuronal dynamics involve a loss of inhibitory signaling in C. elegans

In the aging brain, many of the alterations underlying cognitive and behavioral decline remain opaque. C. elegans offers a powerful model for aging research, with a simple, well-studied nervous system to further our understanding of the cellular modifications and functional alterations accompanying senescence. We perform multi-neuronal functional imaging across the aged C. elegans nervous system, measuring an age-associated breakdown in system-wide functional organization. At single-cell resolution, we detect shifts in activity dynamics toward higher frequencies, alongside a specific loss of inhibitory signaling occurring early in the aging process. These effects are partially delayed or accelerated by a long-lived or neurodegenerative mutant background, respectively. We further provide evidence that these effects are partially mediated through degradation of GABA signaling, via a pathway involving UNC-2/CaV2α and caspase activation. Data from mammals are consistent with our findings, suggesting a conserved shift in the balance of excitatory/inhibitory signaling with age leading to functional decline.

Influence of Tumor Microenvironment and Fibroblast Population Plasticity on Melanoma Growth, Therapy Resistance and Immunoescape

Cutaneous melanoma (CM) tissue represents a network constituted by cancer cells and tumor microenvironment (TME). A key feature of CM is the high structural and cellular plasticity of TME, allowing its evolution with disease and adaptation to cancer cell and environmental alterations. In particular, during melanoma development and progression each component of TME by interacting with each other and with cancer cells is subjected to dramatic structural and cellular modifications. These alterations affect extracellular matrix (ECM) remodelling, phenotypic profile of stromal cells, cancer growth and therapeutic response. The stromal fibroblast populations of the TME include normal fibroblasts and melanoma-associated fibroblasts (MAFs) that are highly abundant and flexible cell types interacting with melanoma and stromal cells and differently influencing CM outcomes. The shift from the normal microenvironment to TME and from normal fibroblasts to MAFs deeply sustains CM growth. Hence, in this article we review the features of the normal microenvironment and TME and describe the phenotypic plasticity of normal dermal fibroblasts and MAFs, highlighting their roles in normal skin homeostasis and TME regulation. Moreover, we discuss the influence of MAFs and their secretory profiles on TME remodelling, melanoma progression, targeted therapy resistance and immunosurveillance, highlighting the cellular interactions, the signalling pathways and molecules involved in these processes.

Divergent Proteomic Responses Offer Insights into Resistant Physiological Responses of a Reef-Foraminifera to Climate Change Scenarios

Reef-dwelling calcifiers face numerous environmental stresses associated with anthropogenic carbon dioxide emissions, including ocean acidification and warming. Photosymbiont-bearing calcifiers, such as large benthic foraminifera, are particularly sensitive to climate change. To gain insight into their responses to near-future conditions, Amphistegina lobifera from the Gulf of Aqaba were cultured under three pCO2 conditions (492, 963, 3182 ppm) crossed with two temperature conditions (28 °C, 31 °C) for two months. Differential protein abundances in host and photosymbionts were investigated alongside physiological responses and microenvironmental pH gradients assessed via proton microsensors. Over 1000 proteins were identified, of which > 15% varied significantly between treatments. Thermal stress predominantly reduced protein abundances, and holobiont growth. Elevated pCO2 caused only minor proteomic alterations and color changes. Notably, pH at the test surface decreased with increasing pCO2 under all light/dark and temperature combinations. However, the difference between [H+] at the test surface and [H+] in the seawater—a measure of the organism’s mitigation of the acidified conditions—increased with light and pCO2. Combined stressors resulted in reduced pore sizes and increased microenvironmental pH gradients, indicating acclimative mechanisms that support calcite test production and/or preservation under climate change. Substantial proteomic variations at moderate-pCO2 and 31 °C and putative decreases in test stability at high-pCO2 and 31 °C indicate cellular modifications and impacts on calcification, in contrast to the LBFs’ apparently stable overall physiological performance. Our experiment shows that the effects of climate change can be missed when stressors are assessed in isolation, and that physiological responses should be assessed across organismal levels to make more meaningful inferences about the fate of reef calcifiers.

Lead Toxicity in Cereals: Mechanistic Insight Into Toxicity, Mode of Action, and Management

Cereals are the major contributors to global food supply, accounting for more than half of the total human calorie requirements. Sustainable availability of quality cereal grains is an important step to address the high-priority issue of food security. High concentrations of heavy metals specifically lead (Pb) in the soil negatively affect biochemical and physiological processes regulating grain quality in cereals. The dietary intake of Pb more than desirable quantity via food chain is a major concern for humans, as it can predispose individuals to chronic health issues. In plant systems, high Pb concentrations can disrupt several key metabolic processes such as electron transport chain, cellular organelles integrity, membrane stability index, PSII connectivity, mineral metabolism, oxygen-evolving complex, and enzymatic activity. Plant growth-promoting rhizobacteria (PGPR) has been recommended as an inexpensive strategy for remediating Pb-contaminated soils. A diverse group of Ascomycetes fungi, i.e., dark septate endophytes is successfully used for this purpose. A symbiotic relationship between endophytes and host cereal induces Pb tolerance by immobilizing Pb ions. Molecular and cellular modifications in plants under Pb-stressed environments are explained by transcription factor families such as bZIP, ERF, and GARP as a regulator. The role of metal tolerance protein (MTP), natural resistance-associated macrophage protein (NRAMP), and heavy metal ATPase in decreasing Pb toxicity is well known. In the present review, we provided the contemporary synthesis of existing data regarding the effects of Pb toxicity on morpho-physiological and biochemical responses of major cereal crops. We also highlighted the mechanism/s of Pb uptake and translocation in plants, critically discussed the possible management strategies and way forward to overcome the menace of Pb toxicity in cereals.

Continuous Exposure to Low Doses of Ultrafine Black Carbon Reduces the Vitality of Immortalized Lung-Derived Cells and Activates Senescence

Combustion-derived nanomaterials are noxious ultrafine (<100 nm) aerosol by-products of human activity. They pose threats to pulmonary health due to their small size, allowing them to penetrate alveoli causing detrimental responses downstream. Information regarding the cellular activity that connects nanocarbon particle exposure to poor pulmonary health remains lacking. We hypothesized that low-dose and long-term administrations of carbonaceous nanoparticles contribute to lung irritation by adversely affecting respiratory cells that function as the first line of defense. Responses to ultrafine black carbon (UBC), a key component of airborne pollutants, by human lung A549, murine lung LA4 epithelial cells, human peripheral-blood monocytes THP1, and murine macrophages RAW264.7 were investigated. The cells were first plated on day zero and were fed fresh UBC suspended in culture media on days one, four, and seven. The exposure regimen included three different concentrations of UBC. On day ten, all cells were harvested, washed, and assayed. The impact on cellular viability revealed that UBC was only moderately cytotoxic, while metabolic activity was significantly diminished in a dose-dependent manner. Additionally, beta-galactosidase proportionally increased with UBC concentration compared to untreated cells, indicating that cellular senescence was promoted across all cell types. The implemented regimen caused minimal toxicity yet demonstrated different cellular modifications across the cell lines of both species, inducing changes to enzyme vitality and cellular fitness. The data suggested that compounding nanosized black carbon exposure could negatively impair overall pulmonary health by distinctively modifying intracellular behavior.