Acute Heat Stress Induces Oxidative Stress and Decreases Adaptation in Young White Leghorn Cockerels by Downregulation of Avian Uncoupling Protein

Abstract

Reactive oxygen species-induced damage of cells and molecules is one of the mechanisms responsible for the decline in an animal's performance due to heat stress. Mitochondria are the main producers of cellular superoxide, a process that is sensitive to proton motive force, and this superoxide production can be decreased by mild uncoupling. We studied the effects of heat stress on the production of mitochondrial superoxide as well as heat stress effects on the expression of avian uncoupling protein (avUCP) and avian A nucleotide translocator (avANT) in skeletal muscles of chicks and young cockerels. Male White Leghorn (Julia) chicks at 16 d and cockerels at 87 d of age were exposed to acute heat stress, 34 degrees C for 18 h, or kept at moderate ambient temperature (25 and 21 degrees C, respectively). There was no difference in mitochondrial superoxide production between heat-exposed and control chicks, whereas significant differences were observed in the case of young cockerels. Greater substrate-independent superoxide production was found in muscle mitochondria from heat-stressed young cockerels. In chicks, neither avUCP nor avANT transcript expression was changed by heat exposure, whereas in young cockerels avUCP transcript was decreased, but avANT transcript level was not changed. Thus, in heat-stressed young cockerels, increased mitochondrial superoxide production was accompanied by downregulation of avUCP. Taken together, these results suggest that exposure of young cockerels to heat stress stimulates mitochondrial superoxide production, possibly via downregulation of avUCP. Chicks with persistent avUCP expression, on the other hand, are relatively better adapted to high temperature. It can be assumed that appropriate expression of avUCP may alleviate overproduction of mitochondrial superoxide and could help birds adapt to oxidative stress resulting from acute heat stress.

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

“…In fact our previous study showed that heat-stressed broiler chickens whose mitochondrial avUCP gene expression and protein levels were downregulated produced more ROS from skeletal muscle mitochondria than control chickens [12]. In contrast, white leghorn cockerels with persistent expression of avUCP on exposure to heat stress showed no change in mitochondrial ROS production [23]. These findings suggest that avUCP may play a key regulatory role in alleviating mitochondrial ROS under heat stress conditions.…”

Scientific Opinion Concerning the Welfare of Animals during Transport

“…In this context acute heat stress has been demonstrated to increase superoxide free radical production in chicken skeletal muscle (Mujahid et al, 2005). This process is mediated by altered mitochondrial function and down-regulation of "uncoupling protein content" (Mujahid et al, 2006(Mujahid et al, , 2007. This mechanism may be responsible for the transport stress and heat stress induced muscle damage and for the changes in muscle and meat quality observed in broilers.…”

Evaluation of anti-coccidial drug sensitivity against experimental coccidiosis in broiler chicks

“…Seven species have been recognized to infect poultry and each species has its own characteristics according to site of infection, immunogenicity and pathogenicity (Williams, 1998;Akhtar et al, 2012). Coccidiosis has been considered as a very harmful disease affecting growth and performance of birds in the intense poultry (Mujahid et al, 2007;Bachaya et al, 2012) and contributory factor in the pathogenesis of several diseases (Shahzad et al,2012). A 3-years recent survey of chicken coccidiosis in Bangladesh showing the severity and persistent problem in poultry farms throughout the country inspite of using various modern anti-coccidial drugs available in the market.…”