Urea as a source of cheap non-protein nitrogen is used to adulterate fish and meat meals which are basic components of broiler diets. The present study was carried out to elucidate the effects of urea on weight gain, ...Urea as a source of cheap non-protein nitrogen is used to adulterate fish and meat meals which are basic components of broiler diets. The present study was carried out to elucidate the effects of urea on weight gain, and hematological and biochemical profiles. A total of 48 broiler chicks were randomly allotted into 4 groups, designated Groups 1, 2, 3 and 4 of 12 birds each. Birds in Groups 2, 3 and 4 were fed on diets containing urea at the levels of 1%, 2.5% and 4%, respectively. Birds in Group 1 served as control and were not exposed to urea. Experimentation period was for 3 weeks and experiment was terminated when birds were 42 days of age. Body weight of all intoxicated birds at the various intervals was significantly decreased in comparison with that of the untreated control. Compared with control, all intoxicated broilers manifested significant (P ≤ 0.05) decrease in all hematological parameters involving erythrocytic and total leucocytic counts, Hemoglobin (Hb) and Packed Cell Volume (PCV) on a dose- and time-pattern. In comparison with the control levels, biochemical profile of the intoxicated birds disclosed significant decrease in blood glucose level and significant increase in serum uric acid, urea, Alkaline Phosphatase (ALP) and Lactate Dehydrogenase (LDH) levels. Based upon the present data, it was concluded that the addition of urea to broiler diets bears serious sequences concerning the general health condition, performance, weight gain, and hematological and biochemical profiles.展开更多
Hypoxia, due to impaired cerebral blood flow, has hazardous effects on brain structure and function. To minimize as much as possible the neurological consequences from hypoxic-ischemic (HI) brain injury, neuro-protect...Hypoxia, due to impaired cerebral blood flow, has hazardous effects on brain structure and function. To minimize as much as possible the neurological consequences from hypoxic-ischemic (HI) brain injury, neuro-protective strategies are urgently required. Vitamin E has been shown to have protective effects against cerebral ischemia, possibly due to its anti-oxidant effects. Thirty albino rats, of both sexes, were obtained from the animal house at King Khalid University Hospital, King Saud University. They were divided into three groups;each included 10 animals: Group A was considered as a control one, animals of Group B were subjected to a permanent link to the carotid arteries on both sides and animals of Group C underwent permanent link to carotid arteries on both sides and concomitantly were given Vitamin E as an anti-oxidant. Animals of Group C were injected by Vitamin E (equivalent to 15 mg/day), into the peritoneal cavity as a single dose for a week and after the prescribed period the mice were sacrificed under deep anesthesia and their brains were extracted and prepared for an electron microscopic study of brain tissue. Specimens from animals of Group B showed a large number of neurons that had been deteriorated. Mitochondria were the most affected organelles. There were a large number of dark cells which probably resulted from shrunken nerve cells and exhibited opaque nuclei. The number of affected nerve cells was much lower in brain tissues from animals of the Group C which revealed absence of dark cells. The study did not disclose any similar changes in brain tissues of the control group animals. Our results suggested that treatment with Vitamin E after hypoxia-ischemia led to a neuro-protective effect that appeared in reduction of cell death of neurons. Thus, the present study provides an evidence that Vitamin E protects the brain tissue of the consequences of hypoxia caused by ischemia in the tested experimental animals. It could be recommended in the treatment of cerebrovascular stroke and neurodegenerative diseases.展开更多
文摘Urea as a source of cheap non-protein nitrogen is used to adulterate fish and meat meals which are basic components of broiler diets. The present study was carried out to elucidate the effects of urea on weight gain, and hematological and biochemical profiles. A total of 48 broiler chicks were randomly allotted into 4 groups, designated Groups 1, 2, 3 and 4 of 12 birds each. Birds in Groups 2, 3 and 4 were fed on diets containing urea at the levels of 1%, 2.5% and 4%, respectively. Birds in Group 1 served as control and were not exposed to urea. Experimentation period was for 3 weeks and experiment was terminated when birds were 42 days of age. Body weight of all intoxicated birds at the various intervals was significantly decreased in comparison with that of the untreated control. Compared with control, all intoxicated broilers manifested significant (P ≤ 0.05) decrease in all hematological parameters involving erythrocytic and total leucocytic counts, Hemoglobin (Hb) and Packed Cell Volume (PCV) on a dose- and time-pattern. In comparison with the control levels, biochemical profile of the intoxicated birds disclosed significant decrease in blood glucose level and significant increase in serum uric acid, urea, Alkaline Phosphatase (ALP) and Lactate Dehydrogenase (LDH) levels. Based upon the present data, it was concluded that the addition of urea to broiler diets bears serious sequences concerning the general health condition, performance, weight gain, and hematological and biochemical profiles.
文摘Hypoxia, due to impaired cerebral blood flow, has hazardous effects on brain structure and function. To minimize as much as possible the neurological consequences from hypoxic-ischemic (HI) brain injury, neuro-protective strategies are urgently required. Vitamin E has been shown to have protective effects against cerebral ischemia, possibly due to its anti-oxidant effects. Thirty albino rats, of both sexes, were obtained from the animal house at King Khalid University Hospital, King Saud University. They were divided into three groups;each included 10 animals: Group A was considered as a control one, animals of Group B were subjected to a permanent link to the carotid arteries on both sides and animals of Group C underwent permanent link to carotid arteries on both sides and concomitantly were given Vitamin E as an anti-oxidant. Animals of Group C were injected by Vitamin E (equivalent to 15 mg/day), into the peritoneal cavity as a single dose for a week and after the prescribed period the mice were sacrificed under deep anesthesia and their brains were extracted and prepared for an electron microscopic study of brain tissue. Specimens from animals of Group B showed a large number of neurons that had been deteriorated. Mitochondria were the most affected organelles. There were a large number of dark cells which probably resulted from shrunken nerve cells and exhibited opaque nuclei. The number of affected nerve cells was much lower in brain tissues from animals of the Group C which revealed absence of dark cells. The study did not disclose any similar changes in brain tissues of the control group animals. Our results suggested that treatment with Vitamin E after hypoxia-ischemia led to a neuro-protective effect that appeared in reduction of cell death of neurons. Thus, the present study provides an evidence that Vitamin E protects the brain tissue of the consequences of hypoxia caused by ischemia in the tested experimental animals. It could be recommended in the treatment of cerebrovascular stroke and neurodegenerative diseases.
