Irreversible impact of early thermal conditions: an integrative study of developmental plasticity linked to mobility in a butterfly species

Within populations, phenotypic plasticity may allow adaptive phenotypic variation in response to selection generated by environmental heterogeneity. For instance, in multivoltine species, seasonal changes between and within generations may trigger morphological and physiological variation enhancing fitness under different environmental conditions. These seasonal changes may irreversibly affect adult phenotypes when experienced during development. Yet, the irreversible effects of developmental plasticity on adult morphology have rarely been linked to life-history traits even though they may affect different fitness components such as reproduction, mobility and self-maintenance. To address this issue, we raised larvae of Pieris napi butterflies under warm or cool conditions to subsequently compare adult performance in terms of reproduction performance (as assessed through fecundity), displacement capacity (as assessed through flight propensity and endurance) and self-maintenance (as assessed through the measurement of oxidative markers). As expected in ectotherms, individuals developed faster under warm conditions and were smaller than individuals developing under cool conditions. They also had more slender wings and showed a higher wing surface ratio. These morphological differences were associated with changes in the reproductive and flight performances of adults, as individuals developing under warm conditions laid fewer eggs and flew larger distances. Accordingly, the examination of their oxidative status suggested that individuals developing under warm conditions invested more strongly into self-maintenance than individuals developing under cool conditions (possibly at the expense of reproduction). Overall, our results indicate that developmental conditions have long-term consequences on several adult traits in butterflies. This plasticity likely acts on life history strategies for each generation to keep pace with seasonal variations and may facilitate acclimation processes in the context of climate change.

Oxidative Stress and Bipolar Mood Disorder: An Important Yet Ambiguous Relationship

Bipolar disorder is a chronic psychological condition that disturbs many patients' lives around the world. The exact pathophysiology of bipolar disorder is yet unknown, but there are several hypotheses to explain this condition. One of the most challenging theories is the role of oxidative stress in the progression of bipolar disorder. Here, we conducted a narrative review to gather the studies that investigated the relationship between bipolar disorder and oxidative stress. We searched PubMed, Scopus, Web of science, and google scholar databases using the following keywords: “bipolar disorder,” “oxidative stress,” “oxidative markers,” and “bipolar patients.” A majority of studies showed that oxidative markers such as Thiobarbituric acid reactive substances are significantly higher in bipolar patients compared to healthy subjects. Based on the included articles, bipolar disorder is associated with oxidative stress. Nevertheless, further well-established Cohorts are required to support these results.

Shenmai Injection Exerts Neuroprotective Functions by Down-regulating MicroRNA-19a in H 2 O 2 -induced PC12 Cells

Background: Acute ischemic stroke (AIS) and following reperfusion therapy-induced cerebral ischemia reperfusion (I/R) injury have been recognized as an important subject of cerebrovascular disease with high mortality. Oxidative stress is an important pathological process of cerebral I/R injury. microRNA-19a (miR-19a) is involved in I/R. As the organ protectant agent, Shenmai Injection (SMI) is widely used in the clinical treatment of cerebral infarction. Purpose: This study aims to explore whether SMI can reduce oxidative stress by regulating miR-19a, thereby treating I/R injury. Methods: The oxidative stress state of PC12 cells was induced by H2O2, and then the cells were cultured with SMI. The therapeutic effect of SMI was evaluated by detecting cellular superoxide dismutase (SOD), malondialdehyde (MDA) and other oxidative markers with the kit. Western blot, PCR, immunofluorescence and other techniques were used to elucidate the potential mechanism of SMI. Results: Cell viability assay results showed that SMI could improve the viability of PC12 cells stimulated by H2O2. Compared with the H2O2 group, after SMI treatment, the contents of MDA and reactive oxygen species (ROS) were significantly reduced, while the activity of SOD was significantly increased, and SMI could reduce apoptosis by increasing the content of adenosine 5'-triphosphate (ATP) in cells and enhancing the mitochondrial membrane potential (∆Ψm). Western blot and qRT-PCR results showed that these effects were partially achieved through the AMPK/Sirt1/PGC-1α pathway. The level of miR-19a was significantly increased in H2O2 group, and SMI could protect the cells by reducing miR-19a. Further investigated the target of miR-19a, and transfected cells with miR-19a mimic and inhibitor respectively. We found that AdipoR2 was a direct target of miR-19a, and miR-19a could inhibit AdipoR2/PI3K/Akt/mTOR pathway. Conclusion:SMI can activate AMPK/Sirt1/PGC-1α and AdipoR2/PI3K/Akt/mTOR pathways by reducing miR-19a levels, and protect PC12 cells stimulated by H2O2.

Association of Oxidative Stress Markers with Vascular Stiffness Parameters in Patients with Diabetic Neuropathy

Introduction: One of the most common chronic complications of diabetes mellitus is diabetic neuropathy. The aim of the study was to elucidate the association between selected markers of oxidative stress and markers of vascular stiffness and to contribute to the understanding of the pathophysiological links between oxidative stress and micro- and macrovascular complications of diabetes. Methods: We enrolled patients with type 2 DM (n = 49), with moderate to severe diabetic polyneuropathy of lower extremities, and a control group without microvascular complications (n = 29). The neuropathy group received alpha-lipoic acid infusion therapy. Sampling was performed before and after treatment to determine the level of oxidative markers (advanced glycation end-products—AGEs, glycation products of AOPP proteins, MDA malondialdehyde and oxidized LDL), parameters of metabolic control and parameters of vascular wall stiffness were measured by sphygmomanometry. Results: After the administration of alpha-lipoic acid, we demonstrated a significant reduction in the level of three selected oxidation markers (AOPP: p < 0.001, AGE: p < 0.001, oxLDL: p < 0.05). In contrast, the level of MDA did not change significantly (p = 0.83). Throughout the group, oxLDL was significantly correlated with central BP (SBP and DBP in the aorta, p < 0.05 and <0.01) and with the augmentation index (AiX/75 bpm, p < 0.01). AOPP significantly correlated with systolic BP in the aorta (p < 0.05). We did not find significant associations in the remaining oxidation markers. Conclusion: In our study, we demonstrated a reduction in the level of oxidative markers after alpha-lipoic acid administration and also an association between markers of oxidative damage to lipids and proteins (oxLDL and AOPP) and some parameters of vascular stiffness.

Salvia spinosa L. Protects against Diabetes-Induced Nephropathy by Attenuation of Mitochondrial Oxidative Damage in Mice

Mitochondrial oxidative damage is a crucial factor in the pathogenesis of diabetic nephropathy (DN), which is among the most prevalent problems of diabetes, and there hasn’t been an effective treatment for DN yet. This study planned to investigate the effects of Salvia spinosa L. on mitochondrial function along with its protection against streptozotocin-induced nephropathy in diabetic mice. After the injection of streptozotocin (STZ) and verification of the establishment of diabetes, mice (n = 30) were randomly divided into the following groups: control group, diabetic-control, S. spinosa-treated diabetic (50, 100, and 200 mg/kg), and metformin-treated diabetic group (500 mg/kg). After four weeks of treatment, the mice were weighed. Blood and kidney tissues were examined for biochemical and histological evaluation. Hematoxylin and eosin staining was used for evaluating renal pathologic damage. Oxidative damage in the kidney was assessed by the evaluation of lipid peroxidation and glutathione oxidation. Furthermore, differential centrifugation was used to obtain the isolated mitochondria, and mitochondrial toxicity endpoints (mitochondrial function and mitochondrial oxidative markers) were determined in them. S. spinosa remarkably reduced the blood urea and creatinine concentrations, and also normalized kidney weight/body weight coefficient in the diabetic mice. S. spinosa ameliorated the incidence of glomerular and tubular pathological changes in histological analyses. Moreover, the oxidative and mitochondrial damages were notably attenuated in renal tissues of S. spinosa-treated mice. These results indicate that the methanolic extract of S. spinosa modulates the nephropathy in the diabetic mice by the amelioration of oxidatively induced mitochondrial damage and provides a reliable scientific base, suggesting S. spinosa as a promising alternative remedy against DN.

On the Antioxidant Properties of L-Kynurenine: An Efficient ROS Scavenger and Enhancer of Rat Brain Antioxidant Defense

L-kynurenine (L-KYN) is an endogenous metabolite, that has been used as a neuroprotective strategy in experimental models. The protective effects of L-KYN have been attributed mainly to kynurenic acid (KYNA). However, considering that L-KYN is prone to oxidation, this redox property may play a substantial role in its protective effects. The aim of this work was to characterize the potential impact of the redox properties of L-KYN, in both synthetic and biological systems. First, we determined whether L-KYN scavenges reactive oxygen species (ROS) and prevents DNA and protein oxidative degradation in synthetic systems. The effect of L-KYN and KYNA (0.1–100 µM) on redox markers (ROS production, lipoperoxidation and cellular function) was compared in rat brain homogenates when exposed to FeSO4 (10 µM). Then, the effect of L-KYN administration (75 mg/kg/day for 5 days) on the GSH content and the enzymatic activity of glutathione reductase (GR) and glutathione peroxidase (GPx) was determined in rat brain tissue. Finally, brain homogenates from rats pretreated with L-KYN were exposed to pro-oxidants and oxidative markers were evaluated. The results show that L-KYN is an efficient scavenger of ●OH and ONOO−, but not O2●– or H2O2 and that it prevents DNA and protein oxidative degradation in synthetic systems. L-KYN diminishes the oxidative effect induced by FeSO4 on brain homogenates at lower concentrations (1 µM) when compared to KYNA (100 µM). Furthermore, the sub-chronic administration of L-KYN increased the GSH content and the activity of both GR and GPx, and also prevented the oxidative damage induced by the ex vivo exposure to pro-oxidants. Altogether, these findings strongly suggest that L-KYN can be considered as a potential endogenous antioxidant.

Effect of Ethanol Leaf Extract of Khat (Catha edulis forsk) on Prefrontal Cortex Oxidative Markers and Hematological Profile of Wistar Rats

Aim: This study evaluated the effect of ethanol leaf extract of Catha edulis on the prefrontal cortex oxidative markers and hematological profile of Wistar rats. Study Design: The study design was experimental. Place and Duration of Study: Department of Biochemistry, Kampala International University, Uganda and Faculty of Medicine, Department of Pharmacy, Mbarara University of Science and Technology, Mbarara, Uganda. Between January and May, 2021. Methodology: Fresh C. edulis leaves were collected after on-spot identification, and authenticated before being chopped into small pieces and pulverized mechanically. The powdered material was extracted through cold maceration using 70% ethanol for 72 h. The extract was concentrated in vacuo to dryness at 40oC using rotary evaporator. The lethal dose (LD50) of the crude extract was determined using acute toxicity test. The sub-acute toxicity of the crude extract was evaluated by orally administering daily doses of 250, 500, and 1000 mg/kg to the male Wistar rats for 28 days. The animals were monitored for mortality, behavioral and physiological signs of toxicity. Superoxide dismutase (SOD), Catalase (CAT) activities and Malondialdehyde (MDA) levels were estimated using standard methods. The blood samples were analyzed using the automated hematology analyzer: Mindray BC-6000. Shenzhen, China. Results: The median lethal dose (LD50) of the C. edulis leaf extract was greater than 5000mg/kg b w. The SOD and CAT activities of C. edulis treated groups compared to the control group were significantly (p < 0.05) reduced, the malondialdehyde (MDA) levels were increased in C. edulis treated groups compared to the control group. There was no significant change in the hematological parameters, however, there were slight variations in the WBC and RBC counts in some C. edulis treated groups. Conclusion: Long term chewing of C. edulis could result in oxidative stress. It is therefore important for chronic C. edulis leaf chewers to take caution.

Effect of combined G6PD deficiency and diabetes on protein oxidation and lipid peroxidation

Background Oxidative Stress, an imbalance in the pro-oxidant/antioxidant homeostasis, occurs in many physiological and non-physiological processes and several human diseases, including diabetes mellitus (DM) and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Since the incidence of G6PD deficiency in Jordan and many parts of the world is high, this study aimed to measure the effect of G6PD deficiency on the oxidative markers and the antioxidant glutathione (GSH) in diabetic and non-diabetic individuals. Methods Whole blood G6PD deficiency was screened by the fluorescent spot method, and erythrocyte G6PD activity was determined using a quantitative assay. Since protein carbonyl (PC) and malondialdehyde (MDA) are the most widely measured markers for protein and lipid oxidation, respectively, plasma PC and MDA, in addition to blood GSH were determined by spectrophotometric assays, as biomarkers of oxidative stress. Results The incidence of G6PD deficiency among the diabetic subjects was 15%. PC level in patients with diabetes and in G6PD-deficient subjects was 5.5 to 6-fold higher than in non-diabetic subjects with sufficient G6PD levels (p<0.001). This fold increase was doubled in diabetic patients with G6PD deficiency (p<0.001). Furthermore, the MDA level was significantly increased by 28-41% in G6PD-deficient, diabetics with sufficient G6PD, and diabetics with G6PD deficiency compared to MDA level in non-diabetic with sufficient G6PD. On the other hand, GSH was significantly reduced to half in G6PD-deficient subjects and in diabetics with G6PD-deficiency. Conclusions The results showed that diabetes and G6PD deficiency increased protein oxidation and lipid peroxidation. However, the combination of both disorders has an additive effect only on protein oxidation. On the other hand, GSH level is only reduced in G6PD deficiency. In addition, diabetes and G6PD deficiency appear to be genetically linked since the incidence of G6PD deficiency among people with diabetes is more than the general population.

Penehyclidine hydrochloride ameliorates renal ischemia reperfusion-stimulated lung injury in mice by activating Nrf2 signaling

Introduction: Penehyclidine hydrochloride (PHC) is an anticholinergic with anti-inflammatory and anti-oxidation activities. PHC displayed protectivity against renal ischemia reperfusion (RIR) injury. Nevertheless, the precise protectivity of PHC on RIR-induced lung injury remains unknown. Methods: We examined the effects of PHC on RIR-induced lung injury and investigated the underlying mechanism. We induced RIR in mice and administrated PHC to RIR mice. Kidney function was monitored by measuring the blood urea nitrogen (BUN) and creatinine level in serum. We evaluated the lung injury, myeloperoxidase (MPO) activity in lung, pro-inflammatory cytokine level, and oxidative markers in serum and lung tissues. We tested the expression level of nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase 1 (HO-1) in lung of RIR mice after PHC treatment. Finally, we evaluated the effects of PHC in RIR Nrf2-/- mice. Results: PHC greatly downregulated the serum levels of BUN, creatinine, IL-6, NO, malondialdehyde (MDA), and matrix metalloproteinase-2. PHC also ameliorated the lung injury, decreased the MPO activity, and suppressed production of IL-6, TNF-α, IFN-γ, MDA, and O2-, while it promoted production of superoxide dismutase (SOD) and catalase (CAT) in lung. PHC improved the production of Nrf2 and HO-1. Conclusion: The protectivity of PHC was absent in Nrf2-/- mice. PHC ameliorated RIR-induced lung injury through Nrf2 pathway.