Mitochondrial energy state controls AMPK-mediated foraging behavior in .

Organisms surveil and respond to their environment using behaviors entrained by metabolic cues that reflect food availability. Mitochondria act as metabolic hubs and at the center of mitochondrial energy production is the protonmotive force (PMF), an electrochemical gradient generated by metabolite consumption. The PMF serves as a central integrator of mitochondrial status, but its role in governing metabolic signaling is poorly understood.

Oocyte mitochondria link maternal environment to offspring phenotype.

During maturation oocytes undergo a recently discovered mitochondrial proteome remodeling event in flies, frogs, and humans. This oocyte mitochondrial remodeling, which includes substantial changes in electron transport chain (ETC) subunit abundance, is regulated by maternal insulin signaling. Why oocytes undergo mitochondrial remodeling is unknown, with some speculating that it might be an evolutionarily conserved mechanism to protect oocytes from genotoxic damage by reactive oxygen species (ROS).

Effect of skeletal muscle mitochondrial phenotype on HO emission.

Reactive oxygen species (ROS) are a key output of the skeletal muscle mitochondrial information processing system both at rest and during exercise. In skeletal muscle, mitochondrial ROS release depends on multiple factors; however, fiber-type specific differences remain ambiguous in part owing to the use of mitochondria from mammalian muscle that consist of mixed fibers. To elucidate fiber-type specific differences, we used mitochondria isolated from rainbow trout (Oncorhynchus mykiss) red and white skeletal muscles that consist of spatially distinct essentially pure red and white fibers.

Mitochondrial complex I ROS production and redox signaling in hypoxia.

Mitochondria are a main source of cellular energy. Oxidative phosphorylation (OXPHOS) is the major process of aerobic respiration. Enzyme complexes of the electron transport chain (ETC) pump protons to generate a protonmotive force (Δp) that drives OXPHOS.

Exhaustive exercise alters native and site-specific HO emission in red and white skeletal muscle mitochondria.

Mitochondrial reactive oxygen species (ROS) homeostasis is intricately linked to energy conversion reactions and entails regulation of the mechanisms of ROS production and removal. However, there is limited understanding of how energy demand modulates ROS balance. Skeletal muscle experiences a wide range of energy requirements depending on the intensity and duration of exercise and therefore is an excellent model to probe the effect of altered energy demand on mitochondrial ROS production.

Factors affecting liver mitochondrial hydrogen peroxide emission.

Mitochondria are key cellular sources of reactive oxygen species (ROS) and contain at least 12 known sites on multiple enzymes that convert molecular oxygen to superoxide and hydrogen peroxide (HO). Quantitation of site-specific ROS emission is critical to understand the relative contribution of different sites and the pathophysiologic importance of mitochondrial ROS. However, factors that affect mitochondrial ROS emission are not well understood.

Anoxia-reoxygenation modulates cadmium-induced liver mitochondrial reactive oxygen species emission during oxidation of glycerol 3-phosphate.

Aquatic organisms are frequently exposed to multiple stressors including low dissolved oxygen (O) and metals such as cadmium (Cd). Reduced O concentration and Cd exposure alter cellular function in part by impairing energy metabolism and dysregulating reactive oxygen species (ROS) homeostasis. However, little is known about the role of mitochondrial glycerol 3-phosphate dehydrogenase (mGPDH) in ROS homeostasis in fish and its response to environmental stress.

Modulation of mitochondrial site-specific hydrogen peroxide efflux by exogenous stressors.

Oxygen (O) deprivation and metals are common environmental stressors and their exposure to aquatic organisms can induce oxidative stress by disrupting cellular reactive oxygen species (ROS) homeostasis. Mitochondria are a major source of ROS in the cell wherein a dozen sites located on enzymes of the electron transport system (ETS) and substrate oxidation produce superoxide anion radicals (O˙‾) or hydrogen peroxide (HO). Sites located on ETS enzymes can generate ROS by forward electron transfer (FET) and reverse electron transfer (RET) reactions; however, knowledge of how exogenous stressors modulate site-specific ROS production is limited.

Assessment of age-related morphological changes in the testes of post-hatch light ecotype Nigerian indigenous chicken.

The age-related morphological changes of the testes in light ecotype Nigerian indigenous chicken were evaluated in this study using gross anatomical, histological and histomorphometric techniques. The results showed that the testes of 3- to 9-month-old birds were light pink while testes of sexually mature chicken were creamy white in colour. The left and right testicular weight, length, diameter, circumference and the organosomatic indices increased significantly (p < .

Effects of monosodium-L-glutamate administration on serum levels of reproductive hormones and cholesterol, epididymal sperm reserves and testicular histomorphology of male albino rats.

This study investigated the effects of administration of monosodium L-glutamate (MSG) on serum gonadotrophin-releasing hormone (GnRH), luteinising hormone (LH), testosterone and total cholesterol (TC), cauda epididymal sperm reserves (CESR) and testicular histomorphology of adult male albino rats. Eighty-four rats, randomly assigned to 7 groups of 12 rats each, were used for the study. Varying low doses (0.