Four Regional Marine Biodiversity Studies: Approaches and Contributions to Ecosystem-Based Management

We compare objectives and approaches of four regional studies of marine biodiversity: Gulf of Maine Area Census of Marine Life, Baltic Sea History of Marine Animal Populations, Great Barrier Reef Seabed Biodiversity Project, and Gulf of Mexico Biodiversity Project. Each program was designed as an "ecosystem" scale but was created independently and executed differently. Each lasted 8 to 10 years, including several years to refine program objectives, raise funding, and develop research networks. All resulted in improved baseline data and in new, or revised, data systems. Each contributed to the creation or evolution of interdisciplinary teams, and to regional, national, or international science-management linkages. To date, there have been differing extents of delivery and use of scientific information to and by management, with greatest integration by the program designed around specific management questions. We evaluate each research program's relative emphasis on three principal elements of biodiversity organization: composition, structure, and function. This approach is used to analyze existing ecosystem-wide biodiversity knowledge and to assess what is known and where gaps exist. In all four of these systems and studies, there is a relative paucity of investigation on functional elements of biodiversity, when compared with compositional and structural elements. This is symptomatic of the current state of the science. Substantial investment in understanding one or more biodiversity element(s) will allow issues to be addressed in a timely and more integrative fashion. Evaluating research needs and possible approaches across specific elements of biodiversity organization can facilitate planning of future studies and lead to more effective communication between scientists, managers, and stakeholders. Building a general approach that captures how various studies have focused on different biodiversity elements can also contribute to meta-analyses of worldwide experience in scientific research to support ecosystem-based management

Amelioration of aluminium-induced liver damage by vitamin E

Objective: To investigate the effects of aluminium sulphate on the microscopic morphology of the liver and on vitamin E amelioration of aluminium-induced liver damage.Methods: Rats were injected intraperitoneally with aluminium sulphate alone or aluminiurn sulphate together with vitamin F, with saline injected rats used as the control group. The study took place in Pamukkale University Faculty of Medicine in 2005.Results: The rats exposed to aluminiurn showed morphological changes in addition to previously reported biochemical changes in the liver. The antioxidant vitamin E significantly diminished the liver damage seen due to aluminium.Conclusion: There is an apparent protective effect of vitamin E on parenteral aluminiurn exposure

hippocampus

Aluminium has toxic effects on many organ systems of the human body. Aluminium toxicity also is a factor in many neurodegenerative diseases. We investigated changes in numbers of hippocampal neurons in rats exposed to aluminium using an optical fractionator and we investigated aluminium-induced apoptosis using the transferase mediated dUTP nick end labeling (TUNEL) assay. Twenty-four female rats were divided equally into control, sham and aluminium-exposed groups. The control group received no treatment. The two treatment groups were injected intraperitoneally with 1 ml 0.9% saline without (sham) and with 3 mg/ml aluminium sulfate every day for two weeks. Following the treatments, the brains were removed, the left hemisphere was used for hippocampal neuron counting using an optical fractionator and the right hemisphere was investigated using hippocampal TUNEL assay to determine the apoptotic index. The number of neurons in the stratum pyramidale of the hippocampus was significantly less in the aluminium group than in the control and sham groups; there was no significant difference between the control and sham groups. The apoptotic index also was significantly higher in the aluminium group than in the other two groups. We quantified the toxic effects of aluminium on the rat hippocampus and determined that apoptosis was the mechanism of aluminium-induced neuron death in the hippocampus

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 mu g 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

diabetic foot injuries

The use of stem or progenitor cells from bone marrow, or peripheral or umbilical cord blood is becoming more common for treatment of diabetic foot problems. These cells promote neovascularization by angiogenic factors and they promote epithelium formation by stimulating cell replication and migration under certain pathological conditions. We investigated the role of CD34 + stem cells from human umbilical cord blood in wound healing using a rat model. Rats were randomly divided into a control group and two groups with diabetes induced by a single dose of 55 mg/kg intraperitoneal streptozocin. Scarred areas 5 mm in diameter were created on the feet of all rats. The diabetic rats constituted the diabetes control group and a diabetes + stem cell group with local injection into the wound site of 0.5 x 106 CD34 + stem cells from human umbilical cord blood. The newly formed skin in the foot wounds following CD34 + stem cell treatment showed significantly improvement by immunohistochemistry and TUNEL staining, and were closer to the wound healing of the control group than the untreated diabetic animals. The increase in FGF expression that accompanied the local injection of CD34 + stem cells indicates that FGF stimulation helped prevent apoptosis. Our findings suggest a promising new treatment approach to diabetic wound healing

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

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

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 mu g 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

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 coad ministration 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 mesengial 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

aluminium

Different forms of Aluminium (Al) are environmental xenobiofics 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 analyaed 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 lu-men. 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