Application Of Theory Of Free Radicals Of Mitochondria During Controlling PHS In Fast-Growing Yellow Broilers

Pulmonary hypertension syndrome (PHS) in broiler chickens poses a serious problem to the international poultry industry, and is an important cause of mortality that has been reported from many parts of the world. For broilers kept at altitudes of approximately 3000m, the onset of pulmonary hypertension, cardiac hypertrophy, heart failure, and oedema leading to PHS has been described. More recently similar symptoms and mortality were reported in broilers reared at lower altitudes of 1000 to 2000m and at altitudes down to sea level. A survey in the United States showed that PHS accounts forover 2-5% of annual broiler losses. An incidence of PHS of 5-10% was reported in China. A global incidence of 4-5% PHS has been reported and, at today's market prices, this mortality represents a cost to the industry of about one billion＄US annually. It has been suggested that the fast-growing modem broiler is particularly susceptible to PHS, because rapid growth causes an increased demand for oxygen, which forces the heart to maintain an elevated cardiac output. The resulting increase in blood pressure within the pulmonary circulation can cause hypertrophy of the fight ventricle and eventually congestive heart failure. This pathogenesis for PHS includes increased oxygen requirements by body tissues and low oxygen tensions in arterial blood. Though a large amount of research about the function of free radicals during the course of pulmonary hypertension syndrome (PHS) in broiler chickens has been done, but what is the mechanism of an internal free radical of mitochondria? What changes does mitochondria function have? Further pathologic mechanism is not clear. The present study was conducted to further evaluate the pathogenesis of the acute and chronic forms of PHS, and to obtain the methods for preventing PHS.A total of 120 commercial broilers were divided randomly into three groups that were respectively treated as control (Group A) and 2 experimental groups (B,C), Broilers in different groups were fed a normal diet before 14 days of age. Then In group B and C, broilers were subjected to a change of temperature by lowering 1～2℃per day from 25℃ (day 14) down to 12℃, and maintained at this ambient temperature until 7 weeks of age. At the same time, 1.5 mg·kg^-1 3, 3, 5-triiodothyronine (T₃) in the diet was added to in groups B in order to induce pulmonary hypertension syndrome (PHS), and 500 mg·kg^-1 ascorbic acid (Vitamin C) in the diet was added to in groups C with the purpose of decreasing the incidence of PHS, Moreover, the liver, heart and mucous membrane of intestine, were taken from 6 killed birds per group at five time points, i. e. after different treatment 1 week,2 weeks,3 weeks,4 weeksand 5 weeks . At every time point, the mitochondria were determined for the evaluations of the concentrations of malondialdehyde (MDA), nitrix oxide(NO) and the activity of nitric oxide synthase (NOS), superoxide dismutase (SOD),glutathione peroxidase (GSH-Px), Na⁺-K⁺—ATPase.The results indicated that1. At 1 and 2 weeks, the MDA level in PHS group decreased significantly (P＜0.05), and the activities ofT-SOD and GSH-Px increased markedly (P＜0.05), of the mitochondria in liver, heart and intestinal mucous membrane. But from 3 weeks to 5 weeks, the MDA level increased significantly, and the activities of T-SOD and GSH-Px decreased markedly (P＜0.05), of the mitochondria in liver, heart and intestinal mucous membrane.After the treatment of Vitamin C, at 1 week, Vitamin C did not significantly increase the MDA level (P＞0.05), of the mitochondria in liver, heart and intestinal mucous membrane in broilers with PHS, Vitamin C didn't significantaly decrease the T-SOD level of the mitochondria in liver and heart (P＞0.05), but changed the T-SOD level of the mitochondria in intestinal mucous membrane. (P＜0.05). and the activities of GSH-Px decreased a little, but not markedly (P＞0.05), of the mitochondria in heart and intestinal mucous membrane, the activities of GSH-Px decreased markedly of the mitochondria in liver (P＜0.05). At 2 weeks, the MDA level increase significantly (P＜0.05), of the mitochondria in liver, and intestinal mucous membrane in broilers with PHS, of the mitochondria in heart, this increase is not significantly (P＞0.05). Vitamin C didn't significantaly decrease the T-SOD level of the mitochondria in liver and intestinal mucous membrane. (P＞0.05), but of the mitochondria in heart decreased significantaly (P＜0.05). and the activities of GSH-Px decreased a little, but not markedly (P＞0.05), of the mitochondria in liver, heart and intestinal mucous membrane, from 3 weeks to 5 weeks, Vitamin C decreased sugnificantly the activity of MDA, of the mitochondria in liver, heart and intestinal mucous membrane in broilers with PHS (P＜0.05) , the T-SOD and GSH-Px level were increased significantly (P＜0.05). It might be concluded that the Pulmonary hypertension syndrome (PHS) in broiler chickens induced markedly the lipid peroxidation of mitochondria and cells, and increased clearly the free radicals, and reduced significantly the antioxidative capacity; the Vitamin C significantly stopped lipid peroxidation induced by PHS, and eliminated markedly productions of a lot of free radicals, and increased significantly the antioxidative capacity.2. From 1 week to 2 weeks, the NO and NOS level of the mitochondria in liver, heart and intestinal mucous membrane in broilers increased significantly (P＜0.05). But from 3 week to 5 week, the NO and NOS level of the mitochondria in liver, heart and intestinal mucous membrane in broilers decreased significantly (P＜0.05).After the treatment of Vitamin C, at lweek, Vitamin C significantly decreased the NO level (P＞0.05), of the mitochondria in liver, heart and intestinal mucous membrane in broilers with PHS, but the NOS level of the mitochondria in liver didn't signifieantaly decrease (P＞0.05), the NOS level of the mitochondria in heartr and intestinal mucous membrane, significantaly decreased (P＜0.05). at 2 weeks, Vitamin C significantly decreased the NO level and NOS level, of the mitochondria in liver, heart and intestinal mucous membrane in broilers with PHS(P＜0.05), From 3 weeks to 5 weeks, the NO level and NOS level, of the mitochondria in liver, heart and intestinal mucous membrane in broilers with PHS were significantly increased.It might be concluded that during the early period of the oxygen deficiting, the activeness of NOS elevates, thus causes the NO level elevate, this diastoles the vessel, alleviates the high pressure of pulmonary artery, is one kind of body stress reaction. But if the oxygen deficiting continuring, body can not react efficiently to alleviate this, thus the adaption comes into being, the synthesize of NOS and NO relatively insufficient, The function of corresponding organ is damaged, the unbalancedly stretch and constringency of the lung blood vessel results the pulmonary artery high pressure, furtherlead to the Pulmonary hypertension syndrome (PHS). It is obviously that medicine has obviously antagonistic role. This can protect the organism.3. At 1 and 2 weeks, the activity of Na⁺-K⁺—ATPase of the mitochondria in PHS group decreased significantly (P＜0.05) , of the mitochondria in liver, heart and intestinal mucous membrane. But from 3 weeks to 5 weeks, the activity of Na⁺-K⁺—ATPase of the mitochondria in liver, heart and intestinal mucous membrane in broilers decreased significantly (P＜0.05).Compared with the PHS group, After the treatment of Vitamin C, at 1 week, Vitamin C significantly decreased the the activity of Na⁺-K⁺—ATPase (P＜0.05), of the mitochondria in liver, but the activity of Na⁺-K⁺—ATPase didn't significantaly decrease (P＞0.05), of the mitochondria in heart and intestinal mucous membrane, at 2 week, Vitamin C significantly decreased the activity of Na⁺-K⁺—ATPase, of the mitochondria in liver, heart and intestinal mucous membrane (P＜0.05), From 3 weeks to 5 weeks, the activity of Na⁺-K⁺—ATPase were significantly increased (P＜0.05), of the mitochondria in liver, heart and intestinal mucous membrane.It might be concluded that the Pulmonary hypertension syndrome (PHS) in broiler chickens induced the damnification of the mitochondria, resulted the disfunction of the energy metabolism, decreased the production of ATP energy, resulted the impediment of the volume, infiltration press, inner environment, ion exchange, and the increase of the blood vessel penetration and the increase of the effusion of the leucocyte and the albumen. Medicine played an important role in the objection of the pulmonary hypertension syndrome (PHS) in broiler chickens and the protection of broilers.4. The cool ambient and dietary T₃ had successfully induced broiler PHS, which was associated with productions of a lot of free radicals and a series of the chain reaction of lipid peroxidation.5. The dietary vitamin C clearly stop the lipid peroxidation, eliminate the free radicals, increase the antioxidative capacity and reduce the incidence of PHS in broilers in the cold ambient and dietary T₃.