ABSTRACT
Seafood in general, shrimps and prawns in particular, are highly nutritious with good source of protein and amino acids. The present study was conducted to evaluate the nutrient value in males and females of green tiger prawn, P. semisulcatus. Twenty specimen were collected from land fisheries in Mediterranean Sea [Alexandria] and from markets [India]. The results showed that the highest values of lipid contents were measured in the female and male edible muscles [P. semisulcatus at Mediterranean Sea [Alexandria] compared to female and male edible muscles of the same species from market [India]. The carbohydrate contents in the male edible muscles of P. semisulcatus were higher compared to females in the studied regions. Sixteen amino acids have been determined in edible muscle of P. semisulcatus, among these, nine essential amino acids [EAAs] and seven non- essential amino acids [NEAAs] were estimated in both sexes from two regions. The quantities of amino acids vary considerably between sexes. The fatty acid contents from the muscles of the P. semisulcatus showed the presence of fifteen individual fatty acids, which include seven saturated fatty, three mono and five polyunsaturated fatty acids [MUFA and PUFA]. Twelve protein bands were detected in males of P. semisulcatus [12 bands]; while the females had 13 bands from market [India] compared to 9 bands of both males and females from Mediterranean Sea [Alexandria].Conclusion: The present study clearly indicated that the nutritional value of P. semisulcatus is very well as food and health care
ABSTRACT
2-Butoxyethanol [2-BE] is a clear colorless liquid that smells like ether. It is used as a solvent in spray lacquers, varnishes, varnish removers, herbicides, liquid soaps, cosmetics, industrial and household cleaners, and dry-cleaning compounds. 2-BE causes cellular damage via formation of reactive oxygen species. Acacia nilotica [A.nilotica] leaf extract exhibited significant antimutagenic and DNA-protective effects against oxidative damage due to the presence of alkaloids, volatile essential oils, phenols and phenolic glycosides; it is considered an excellent free radical scavenging antioxidant owing to the high number of hydroxyl groups. Silymarin [SIL] is a standardized mixture of antioxidant flavonolignans [silybin and silibinin]. Silybum marianum [Milk thistle] family Asteraceae is an ancient medicinal plant from which SIL is extracted. It is a free radical scavenger and a membrane stabilizer that prevents lipid peroxidation. In the present study, we investigated the effects of extracts of A.nilotica leaves and SIL on the toxicity of 2-BE
Materials and Methods: 2-BE was given orally to male albino mice for 28 days at dose [450microl/kg b.wt]. A. nilotica leaf extract [25 mg/kg b.wt] was dissolved in water and was administered orally for 14 days prior to 28 days treatment of 2-BE and during the 28 days. Also SIL [20 mg/kg b.wt] was administered orally for 14 days prior to 28 days treatment of 2BE and during the 28 days
Result: In the present work, genotoxic effects were induced by 2-BE through oral administration, and the protective effect of A. nilotica and SIL are studied. 2-BE induced a significant increase in the structural as well as numerical chromosomal aberrations. The frequency of chromosomal aberrations showed significant decrease when mice treated with A. nilotica extract and SIL. Also, there were significant increases in micronuclei. A. nilotica extract and SIL administration significant decreases micronuclei induced by 2-BE. However 2-BE induced a significant decrease in mitotic index. Administration of both A. nilotica extract and SIL significant increase mitotic index in mice treated with 2-BE. Exposure of mice to 2-BE caused significant changes in the hematological paramters as well as significant increases in the activities of serum enzymes alanine aminotransferases [ALAT], aspartate aminotransferases [ASAT] and alkaline phosphatase [ALP]. Also, 2-BE induced a significant decrease in the content of liver reduced glutathione [GSH], however, induced a significant increase in the level of hepatic lipid peroxidation end product [MDA] of male mice. Coadministration of both A. nilotica extract and SIL to 2-BE-intoxicated mice ameliorated the above-mentioned parameters
Conclusion: 2-BE induced mutagenic and liver injury in male mice. A.nilotica and SIL are found to reduce the percentage of chromosomal aberration and micronuclei cells as they are a powerful antioxidant, they are able to scavenger reactive oxygen species [free radicals] formed by 2-BE in the cells, these free radicals damage DNA and hence cause defects in the chromosomes. A. nilotica extract and SIL could be used as a protective agent against mutagenic and hepatic injuries resulting from 2-BE. The protective action of SIL is more effective than A. nilotica
ABSTRACT
Previous studies demonstrated the hepatotoxicity of thioacetamide [TAA] in rats. The present study is a trial to decline TAA-hepatotoxicity by using the roots of herbal medicinal plant [Panax ginseng] pre-treatment . Low dose of TAA [50-mg/kg b.wt] was chosen to induce hepatoxicity in male rats previously treated with ginseng for 10 consecutive days. The tested parameters were studied after 24, 48 and 72 hours post TAA intoxication. Fluctuatious of serum glucose were noticed in TAA intoxicated rats increased after 24 h [+ 9.31%], 48h. [+ 7.11%], followed by moderate improvement after 72 h. [+5.39%] when compared with control group. Ginseng pretreatment enhanced these changes towards the normal values. Serum and liver enzyme activities [AST, AIT, ALP and ? GT] increased in TAA intoxicated rats which peaked after 48 h, and began to decrease after 72h. Pretreatment with ginseng improved enzyme activities to some extent. Reduced glutathione [GSH] as well as antioxidant enzyme glutathione reductase [GSH-R] activity while lipid peroxidation [LPO] increased in TAA intoxicated rats and enhanced by pretreatment with ginseng. This results suggest that pretreatment with ginseng could improve the detoxifying activity of the liver rats with TAA-induced acute hepatotoxicity