1,3-butanediol administration as an alternative strategy to calorie restriction for neuroprotection - Insights into modulation of stress response in hippocampus of healthy rats.

Ketogenic diet has a wide range of beneficial effects but presents practical limitations due to its low compliance, hence dietary supplements have been developed to induce ketosis without nutrient deprivation. The alcohol 1,3-butanediol (BD) is a promising molecule for its ability to induce ketosis, but its effects on brain have been investigated so far only in disease models, but never in physiological conditions. To support BD use to preserve brain health, the analysis of its activity is mandatory.

Rapid modulation of interscapular brown adipose tissue mitochondrial activity by ketosis induced by 1,3-butanediol administration to rats.

Some studies indicate that brown adipose tissue (BAT) represents a promising target in the fight against dysmetabolic diseases, with indications suggesting it as a potential target for the effects of ketone bodies. We investigate whether the elevation of plasma levels of the ketone body β-hydroxybutyrate, achieved through the in vivo administration of its precursor 1,3-butanediol (BD) to rats, could impact interscapular BAT (iBAT) mitochondrial biochemistry and functionality. We examined the effects induced by BD within 3 h and after 2 weeks of treatment.

Simultaneous induction of systemic hyperglycaemia and stress impairs brain redox homeostasis in the adult zebrafish.

For diabetic patients it is crucial to constantly monitor blood glucose levels to mitigate complications due to hyperglycaemia, including neurological issues and cognitive impairments. This activity leads to psychological stress, called "diabetes distress," a problem for most patients living with diabetes. Diabetes distress can exacerbate the hyperglycaemia effects on brain and negatively impact the quality of life, but the underlying mechanisms remain poorly explored.

Polystyrene microplastics effects on zebrafish embryological development: Comparison of two different sizes.

Microplastics have become a great worldwide problem and it's therefore important to study their possible effects on human and environmental health. In this study, zebrafish embryos were used to compare two different sizes of polystyrene microplastics (PS-MPs), 1 µm and 3 µm respectively, at 0.01, 0.

Effects of Dibutylphthalate and Steroid Hormone Mixture on Human Prostate Cells.

Phthalates are a family of aromatic chemical compounds mainly used as plasticizers. Among phthalates, di-n-butyl phthalate (DBP) is a low-molecular-weight phthalate used as a component of many cosmetic products, such as nail polish, and other perfumed personal care products. DBP has toxic effects on reproductive health, inducing testicular damage and developmental malformations.

Changes in the Mitochondria in the Aging Process-Can α-Tocopherol Affect Them?

Aerobic organisms use molecular oxygen in several reactions, including those in which the oxidation of substrate molecules is coupled to oxygen reduction to produce large amounts of metabolic energy. The utilization of oxygen is associated with the production of ROS, which can damage biological macromolecules but also act as signaling molecules, regulating numerous cellular processes. Mitochondria are the cellular sites where most of the metabolic energy is produced and perform numerous physiological functions by acting as regulatory hubs of cellular metabolism.

1,3-Butanediol Administration Increases β-Hydroxybutyrate Plasma Levels and Affects Redox Homeostasis, Endoplasmic Reticulum Stress, and Adipokine Production in Rat Gonadal Adipose Tissue.

Ketone bodies (KBs) are an alternative energy source under starvation and play multiple roles as signaling molecules regulating energy and metabolic homeostasis. The mechanism by which KBs influence visceral white adipose tissue physiology is only partially known, and our study aimed to shed light on the effects they exert on such tissue. To this aim, we administered 1,3-butanediol (BD) to rats since it rapidly enhances β-hydroxybutyrate serum levels, and we evaluated the effect it induces within 3 h or after 14 days of treatment.

Aluminum induces a stress response in zebrafish gills by influencing metabolic parameters, morphology, and redox homeostasis.

Environmental air pollution and resulting acid rain have the effect of increasing aluminum levels in water bodies. We studied the effects of aluminum on fish gills, the tissue most exposed to aluminum, using zebrafish as an experimental model. Adult zebrafish were exposed to an aluminum concentration found in polluted environments (11 mg/L) for 10, 15 and 20 days and the effects on gill morphology, redox homeostasis (ROS content, NADPH oxidase, NOX, activity, oxidative damage, antioxidant enzymes, total antioxidant capacity, in vitro susceptibility to oxidants) and on behavioural and metabolic parameters (routine respiratory oxygen consumption rMO, tail-beating frequency, cytochrome oxidase activity and muscle lactate content) were evaluated.

Muscle Oxidative Stress Plays a Role in Hyperthyroidism-Linked Insulin Resistance.

While a low level of ROS plays a role in cellular regulatory processes, a high level can lead to oxidative stress and cellular dysfunction. Insulin resistance (IR) is one of the dysfunctions in which oxidative stress occurs and, until now, the factors underlying the correlation between oxidative stress and IR were unclear and incomplete. This study aims to explore this correlation in skeletal muscle, a tissue relevant to insulin-mediated glucose disposal, using the hyperthyroid rat as a model of oxidative stress.

Effects of superoxide anion attack on the lipoprotein HDL.

High-density lipoprotein (HDL) is an anti-atherosclerotic lipoprotein. Thanks to the activity of apolipoprotein ApoA1, the principal protein component of HDL, this last is responsible for converting cholesterol into ester form and transporting excessive cholesterol to the liver ("reverse cholesterol transport" RCT). When HDL undergoes oxidation, it becomes dysfunctional and proatherogenic.

Hepatic Insulin Resistance in Hyperthyroid Rat Liver: Vitamin E Supplementation Highlights a Possible Role of ROS.

Thyroid hormones are normally involved in glycaemic control, but their excess can lead to altered glucose metabolism and insulin resistance (IR). Since hyperthyroidism-linked increase in ROS results in tissue oxidative stress that is considered a hallmark of conditions leading to IR, it is conceivable a role of ROS in the onset of IR in hyperthyroidism. To verify this hypothesis, we evaluated the effects of vitamin E on thyroid hormone-induced oxidative damage, insulin resistance, and on gene expression of key molecules involved in IR in the rat liver.

Environmental concentrations of a delorazepam-based drug impact on embryonic development of non-target Xenopus laevis.

Benzodiazepines, psychotropics drugs used for treating sleep disorders, anxiety and epilepsy, represent a major class of emerging water pollutants. As occurs for other pharmaceutical residues, they are not efficiently degraded during sewage treatment and persist in effluent waters. Bioaccumulation is already reported in fish and small crustaceans, but the impact and consequences on other "non-target" aquatic species are still unclear and nowadays of great interest.

Oxidative damage and mitochondrial functionality in hearts from KO UCP3 mice housed at thermoneutrality.

The antioxidant role of mitochondrial uncoupling protein 3 (UCP3) is controversial. This work aimed to investigate the effects of UCP3 on the heart of mice housed at thermoneutral temperature, an experimental condition that avoids the effects of thermoregulation on mitochondrial activity and redox homeostasis, preventing the alterations related to these processes from confusing the results caused by the lack of UCP3. WT and KO UCP3 mice were acclimatized at 30 °C for 4 weeks and hearts were used to evaluate metabolic capacity and redox state.

Mitochondrial Management of Reactive Oxygen Species.

Mitochondria in aerobic eukaryotic cells are both the site of energy production and the formation of harmful species, such as radicals and other reactive oxygen species, known as ROS. They contain an efficient antioxidant system, including low-molecular-mass molecules and enzymes that specialize in removing various types of ROS or repairing the oxidative damage of biological molecules. Under normal conditions, ROS production is low, and mitochondria, which are their primary target, are slightly damaged in a similar way to other cellular compartments, since the ROS released by the mitochondria into the cytosol are negligible.

Dietary Supplementation Increases Antioxidant Capacities and Reduces Ros Release in Mitochondria of Hyperthyroid Rat Liver.

The ability of aerobic organisms to cope with the attack of radicals and other reactive oxygen species improves by feeding on foods containing antioxidants. Microalgae contain many molecules showing in vitro antioxidant capacity, and their food consumption can protect cells from oxidative insults. We evaluated the capacity of dietary supplementation with 1% dried strain 211/8k, an alga rich in glutathione, α-tocopherol, and carotenoids, to counteract an oxidative attack in vivo.

Vitamin E Supplementation and Mitochondria in Experimental and Functional Hyperthyroidism: A Mini-Review.

Mitochondria are both the main sites of production and the main target of reactive oxygen species (ROS). This can lead to mitochondrial dysfunction with harmful consequences for the cells and the whole organism, resulting in metabolic and neurodegenerative disorders such as type 2 diabetes, obesity, dementia, and aging. To protect themselves from ROS, mitochondria are equipped with an efficient antioxidant system, which includes low-molecular-mass molecules and enzymes able to scavenge ROS or repair the oxidative damage.

24S-hydroxycholesterol affects redox homeostasis in human glial U-87 MG cells.

The cholesterol metabolite 24(S)-hydroxycholesterol (24S-OHC) allows cholesterol excretion from the brain and was suggested to be critically involved in physiological as well as neurodegenerative processes. It induces on human neuronal cell cultures a dose dependent toxicity associated with increased reactive oxygen species production. Since glial cells play a key role in assisting neuronal function, here we investigated the effects of increased concentrations of 24S-OHC on a glial cell model (human glioblastoma U-87 MG cells).

Thyroid state affects HO removal by rat heart mitochondria.

We investigated the effects of thyroid state on the mechanisms underlying rat heart mitochondrial capacity to remove HO produced by an exogenous source. The removal rates were higher in the presence of respiratory substrates independently from thyroid state and were higher in hyperthyroid than in hypothyroid preparations. The thyroid state-linked changes in HO removal rates, mirrored those in HO release rates, showing that endogenous and exogenous HO do not compete for the removing system.