The suppressive effect of dietary coenzyme Q on mitochondrial reactive oxygen species production and oxidative stress in chickens exposed to heat stress.

This study was conducted to determine if dietary supplementation with coenzyme Q (CoQ ), which can act as a potent antioxidant and is an obligatory cofactor of mitochondrial uncoupling protein, suppresses the heat stress (HS)-induced overproduction of mitochondrial reactive oxygen species (ROS) and oxidative damage in the skeletal muscle of birds. The carbonyl protein content of skeletal muscle was significantly higher in birds exposed to HS treatment (34°C, 12 h) than in thermoneutral birds (25°C). This increase was suppressed by CoQ supplementation (40 mg/kg diet).

Acute cold-induced thermogenesis in neonatal chicks (Gallus gallus).

Mechanisms of thermogenic responses that play a role to maintain homeothermy during an early stage of neonatal chicks on acute cold exposure are scarcely studied as hatchlings are believed to be poikilothermic. However, chicks can attain the homeothermy during their subsequent growth after hatching. To identify thermogenic responses during neonatal stages of chicks (Gallus gallus) on acute cold exposure (12 degrees C, 3h), changes in plasma corticosterone levels, thermogenesis, gene transcripts (avUCP and avPGC1alpha) in skeletal muscles (pectoralis superficialis and gastrocnemius) and mitochondrial substrate oxidation enzyme activities in dissected tissues of 1- and 4-d-old chicks were studied.

Olive oil-supplemented diet alleviates acute heat stress-induced mitochondrial ROS production in chicken skeletal muscle.

We have previously shown that avian uncoupling protein (avUCP) is downregulated on exposure to acute heat stress, stimulating mitochondrial reactive oxygen species (ROS) production and oxidative damage. In this study, we investigated whether upregulation of avUCP could attenuate oxidative damage caused by acute heat stress. Broiler chickens (Gallus gallus) were fed either a control diet or an olive oil-supplemented diet (6.

Oxidative damage in different tissues of neonatal chicks exposed to low environmental temperature.

Maintenance of body temperature in a cold environment is crucial for survival in homeotherms. However, we have previously reported that on exposure to low environmental temperature, neonatal chicks (Gallus gallus) show hypothermia, decreased behavioral activity, and absence of gene transcript enhancement of putative thermogenic proteins, as well as no change in mitochondrial substrate oxidation enzymes. Various metabolic abnormalities and/or tissue damage may also decline the thermogenic capacity of low-temperature-exposed neonatal chicks.

Central administration of corticotropin-releasing factor induces tissue specific oxidative damage in chicks.

Corticotropin-releasing factor (CRF) modulates the activity of the hypothalamic-pituitary-adrenal (HPA) axis, and has a key role in mediating neuroendocrine effects which occur in response to stressful stimuli. We have recently shown that intracerebroventricular (ICV) injection of CRF in neonatal chicks increased homeothermy that was associated with enhanced gene transcripts of mitochondrial fatty acid (FA) transport and oxidation enzymes in a tissue specific manner. These observations prompted an investigation into the potential role of CRF in a state of oxidative damage in different tissues.

Homeothermy in neonatal chicks exposed to low environmental temperature with or without intracerebroventricular administration of corticotropin-releasing factor.

To determine the mechanism of sensitivity to low-temperature exposure (20 degrees C for 3h) and corticotropin-releasing factor (CRF) induced increased homeothermy, we investigated gene transcripts of putative thermogenic proteins and mitochondrial fatty acid (FA)-oxidation enzymes in neonatal chicks. The hypothalamic-pituitary-adrenal (HPA) axis in low-temperature-exposed neonatal chicks was activated by central administration of CRF. Neonatal chicks showed hypothermia on exposure to low-temperature, with no enhancement of HPA axis and gene transcripts of avian adenine nucleotide translocator, avian uncoupling protein, avian peroxisome-proliferator-activated receptor-gamma co-activator-1alpha, and mitochondrial FA transport and oxidation enzymes in vital organs.

Sequential changes in superoxide production, anion carriers and substrate oxidation in skeletal muscle mitochondria of heat-stressed chickens.

We have shown that heat-stressed birds exhibit increased superoxide production in skeletal muscle mitochondria. To determine the precise mechanism for this effect, here we studied not only progressive, but also sequential changes in superoxide production, anion carriers and substrate oxidation in mitochondria of heat-stressed chickens. Exposure to acute heat stress (34 degrees C for 6, 12 and 18h) stimulated pectoralis muscle mitochondrial superoxide production.

Possible role of avian uncoupling protein in down-regulating mitochondrial superoxide production in skeletal muscle of fasted chickens.

Little is known about the precise physiological roles of uncoupling protein 1 (UCP1) homologs (UCP2, UCP3, avian UCP) whose levels are up-regulated during fasting. UCPs in skeletal muscle are thought to play a role in the regulation of lipids as fuel substrates, and/or in controlling the production of reactive oxygen species (ROS). The aim of this investigation, using skeletal muscle from fasted chickens, was to examine alterations in the expression of genes encoding for avian UCP and key enzymes relevant to lipid flux across the mitochondrial beta-oxidation pathway.