Aluminium sulphate exposure increases oxidative stress and suppresses brain development in Ross broiler chicks.

BACKGROUND: Aluminium (Al) is known to have neurotoxic effects that can result in oxidative damage to a range of cellular biomolecules. These effects appear to be of significance in the developmental stages of the brain. We therefore investigated the oxidative and histopathological damage induced by Al during growth and development of the chick brain. MATERIAL/METHODS: We used a chick embryonic development model, with Al treatment of 500 µg Al sulphate in 0.1 ml saline injected into the egg air chambers at the beginning of their incubation period. The effects on chick-brain growth and development were then assessed at term (day 21). Determination of malondialdehyde and glutathione levels were used as relevant biological measures for increased oxidative stress in terms of lipid peroxidation and biochemical oxidative damage, respectively. Furthermore, we also monitored neuronal degeneration as estimated stereologically using the Cavalieri brain volume estimation tool. RESULTS: This Al treatment showed significantly increased MDA levels and decreased GSH levels, as indicators of increased biochemical oxidative damage. This was accompanied by significantly decreased brain volume, as a measure of neuronal degeneration during brain development in this chick embryonic development model. CONCLUSIONS: Exposure to Al during chick embryonic development results in increased oxidative stress in the brain that is accompanied by neuronal degeneration.

The effects of copper sulfate on liver histology and biochemical parameters of term Ross broiler chicks.

Copper is an essential trace element that is extremely toxic to organisms and organs at high doses. We have investigated the histological and biochemical effects of a toxic dose of copper sulfate on the liver of term Ross broiler chicks. Fertilized eggs were divided into three groups: experimental, injected with 50 mcg/0.1 ml copper sulfate in the air chambers on day 1; sham, injected with 0.1 ml saline; and control, no injection. Term chicks were killed and their livers investigated histologically, with hematoxylin-eosin-stained sections examined under light microscopy, and biochemically, for malondialdehyde and glutathione levels. Histological examinations showed copper-treated samples with granular degeneration and necrosis of hepatocytes and impairment to the cell lining of the remark cords. The samples had a congestive appearance, with blood in the vena centralis and sinusoids, slight connective tissue increase, and lymphocyte infiltration. Control and sham group sections had normal appearances. As oxidative damage parameters, in the copper-treated group, malondialdehyde levels were increased and glutathione levels decreased. In the sham and control groups, there were no significant differences. At this toxic dose, copper sulfate shows oxidative damage according to the histology of term chick liver that are confirmed biochemically by the changes in malondialdehyde and glutathione levels.

Morphology, and muscle- and papilla-volume ratios, of the tongue of Laudakia stellio (Agamidae, Squamata): a histological and stereological study.

We examined the histological structure of the tongue of Laudakia stellio, the starred agama lizard (Agamidae, Squamata), under light microscopy. We also investigated the muscle and papilla volume ratios, with volumes of each aspect of interest estimated according to the Cavalieri method. The macroscopically short, thick and muscle-rich front tip of the tongue of L. stellio does not show any bifurcation, and under light microscopy, the oval-shaped papilla-free front tip was seen to be covered by keratinized stratified epithelium. The dorsal and ventral parts were different, with the former partially covered by keratinized stratified epithelium and rich in secretory glands and secretory cells. The ventral part, which contained keratinized stratified cells, had a flat surface with no papillae. The dorsal surface of the anterior and posterior parts contained fungiform papillae, with the apical parts of these papillae containing minimal keratin; the interpapillar space was covered by keratin-free squamous stratified epithelium. The middle section of the tongue contained cylindrical-type papillae, with serous and mucous secretory glands and ducts at their base. Finally, the frontal and middle parts of the ventral and dorsal surfaces did not contain any taste buds, although there were some in the hind part of the dorsal surface. As morphometric estimates of volumes of the muscles and papillae, the mean volume ratios (relative to total tongue volume)+/-standard deviation were 0.66+/-0.03 and 0.33+/-0.03, with mean coefficients of error of 0.02 and 0.03, respectively.

Vitamin E protection from testicular damage caused by intraperitoneal aluminium.

Different forms of Aluminium (Al) are environmental xenobiotics that induce free radical-mediated cytotoxicity and reproductive toxicity. Vitamin E (alpha -tocopherol) is an antioxidative agent that has been reported to be important for detoxification pathways. This study was thus aimed at elucidating the protective effects of vitamin E towards aluminium toxicity on the histology of the rat testis. Al (5 mg/kg body weight) was administered intraperitoneally in 2 ml saline, either alone or immediately before vitamin E (500 mg/kg body weight), at a different point of abdomen, and the alterations in the testis tissue were analyzed histologically. Seven treated animals were sacrificed for each group, with the testes removed and examined histologically. In the Al-treated group, the germinal epithelium of the seminiferous tubules was thinner in places and spermatids were almost absent; sperm numbers were low and there were no sperm in the lumen. In the Al plus vitamin E rats, there were large numbers of spermatids and sperm in the seminiferous tubule lumen. In the vitamin E alone group, a normal histology was seen. Electron microscopically, in the Al-treated group there were irregularities in the nuclear membrane, some damaged mitochondria, a decrease in the number of ribosomes, and an increase in the number of lysosomes in the sertoli cell cytoplasm. In the primary spermatocyte cytoplasm, there was an increase in the rough endoplasmic reticulum. In the Al plus vitamin E group, the spermatogeneic cells and the sertoli cell cytoplasm showed an almost normal appearance. The ultrastructure of the testis in the vitamin E alone group showed a normal appearance. In conclusion, vitamin E antagonizes the toxic effects of Al at the histological level, thus potentially contributing to an amelioration of the testis histology in the Al-treated rats. The associated biochemical parameters merit further investigation.

Histological and ultrastructural evidence for protective effects on aluminium-induced kidney damage by intraperitoneal administration of alpha-tocopherol.

The nephrotoxic actions of aluminium (Al) arise from its accumulation in the kidneys, with the resultant degeneration of the renal tubular cells. It has been suggested that Al generates reactive oxygen species that cause the oxidative deterioration of cellular lipids, proteins, and DNA. To test this hypothesis, we have here investigated the potential for a protective role of alpha-tocopherol (vitamin E) during short-term exposure of rats to Al. Al was administered intraperitoneally either alone or in combination with vitamin E at a different point of abdomen, and the alterations in the kidney tissue were analyzed histologically. The results reveal that significant light microscopical and ultrastructural damage is caused by Al, whereas with the immediate coadministration of vitamin E, there is a protective effect against this damage to the kidney tissue. In Al-alone group, the glomeruli and proximal tubuli and the Bowman capsules had swellings, adherence, hemorrhage, increase in mesangial matrix, and marked interstitial tissue fibrosis, indicating severe damage. In the Al and vitamin E immediate coinjected group, renal tubule cells were almost of a normal appearance. A slight stenosis was seen in the capsular area in the Malpighi corpuscules. The tubular organization and the cytoplasmic basophilia were also much the same as in the control group, with the lumen clearly visible in most of the cortical tubuli. The results highlight the need to reduce exposure to Al, with particular attention being paid to the known sources of Al. At the same time, the maintenance of a diet that is rich in vitamin E should be beneficial in the alleviation of Al toxicity.

Neuroprotective effects of L-carnitine and vitamin E alone or in combination against ischemia-reperfusion injury in rats.

BACKGROUND: Neurological injury because of transient cerebral ischemia is a potential complication of cardiovascular surgery. In this study, the neuroprotective effects of L-carnitine, vitamin E, and the combination of these agents on ischemia/reperfusion (I/R) injury were determined in a rat model of transient global cerebral I/R. METHODS: Rats were pretreated with L-carnitine (100 mg/kg, i.v.) and vitamin E (50 mg/kg, i. v.), alone or in combination and then subjected to cerebral I/R induced by a four-vessel-occlusion technique for a duration of 15 min followed by 15 min of reperfusion. Malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, and glutathione (GSH) levels were measured in the cerebral tissues. Histopathological examinations were also carried out under light and electron microscopy. RESULTS: The results showed that I/R elevated MDA levels, which were accompanied by a reduction in SOD activities and GSH levels. Surviving neurons was markedly decreased in CA1 and CA3 subfield of hippocampus in I/R animals. L-carnitine, vitamin E, and their combination restored MDA levels and SOD activities, with a tendency to increase surviving neurons in CA1 and CA3 subfield. Combined treatment of L-carnitine and vitamin E had better GSH levels than individual treatment of these agents. CONCLUSIONS: The results suggest that L-carnitine has a potent neuroprotective effect against cerebral-I/R-induced injury in rat brain that is comparable to that of vitamin E. However, the combined use of L-carnitine and vitamin E does not further protect from neuronal injury, although it provides an increase in GSH levels.