الفهرس 
Pathological and bacteriological studies in some fishes implicated in histamine food poisoning with experimental trials for protection using fractions of green tea extracts in rats
AbstractOnly 14 pages are availabe for public view
 |  | from | 305 |  |  |
| | | from | 305 | | |
Abstract
The current study was divided into two experiments. The first experiment aimed to investigate the effect of storage time and temperature on muscular histamine (HIS) contents in both little tunny (Euthynnus alletteratus) and sardine (Sardina Pilchardus). 100 fresh little tunny and sardine were divided into two groups (n=50). group (1) preserved in crushed ice (0°C) and group (2) was kept at room temperature (21°C). The freshness of all fishes was evaluated at 0, 6, 12, 18, and 24 h post-fishing using Quality Index Method (QIM) and European Union (EU) grading scheme. Muscles from abdominal, dorsal and tail areas were collected at the same time intervals for histopathology, immunohistochemistry, histamine analysis and bacteriological study. The second experiment was designed to evaluate the potential mechanisms underlying HIS toxicity in rats and to explore the possible protective effect of epigallocatechin gallate- rich fraction (EGCGR) against such toxicity. In the toxicity study, we used 40 adult male albino Wistar rats that divided into 4 groups (n= 10). group (1) was received distilled water, groups (2&3) were received HIS at 250- and 500 mg/kg BWT/day, respectively and group (4) was received HIS at 1750 mg/kg BWT/week. All treatments were taken oral for two weeks. Meanwhile, we used 30 adult male rats to evaluate the protective potential of EGCGR against acute and subacute HIS-toxicity. Rats were divided in to 6 groups (n=5) as follows: (1) distilled water; (2&3) EGCGR at 100- and 200 mg/kg BWT/ day), respectively; (4) HIS at 1750 mg/g BWT/week; and (5&6) HIS + EGCGR at the same frequency and doses that mentioned previously. Our results showed marked increase in fish deterioration associated with a significant increase in both HIS levels and HIS-forming bacterial (HFB) count in different muscle areas throughout storage time and temperatures. All the measuring parameters were recorded the highest levels in the abdominal muscle followed by tail then dorsal muscle. We localized HIS and gram-negative bacteria all over the muscular tissue mainly in the intermuscular space, myofibrils and surrounding the blood vessels. Additionally, we found that continuous oral administration of HIS for 14 days significantly induced neuronal and cardiopulmonary toxicity in rats. HIS also induced dose- and time dependent oxidative stress manifested by increase in the MDA levels and reduce CAT activity and GSH levels in the brain, lung and heart tissues. The microscopic picture of the affected tissues showed extensive cellular degeneration and necrosis along with severe inflammatory reactions. There was a significant increase in both gene and protein expression of casp-3, bax, JNK, c-Fos c-Myc, c-Jun, NF-B, TNF- IL-1, iNOS, and Cox2 along with downregulation of Bcl2 gene in all the examined organs. On the other hand, the cotreatment of EGCGR with HIS could alleviate all the above-mentioned toxicological parameter. We suggest that the oxido-inflammatory stress plays a pivotal role in HIS-inducing both neuronal and cardiopulmonary toxicity in rats. Furthermore, EGCGR exerts a potent antihistaminic effect either directly or indirectly via its anti-inflammatory, antioxidant and antiapoptotic properties.