This study determined the presence of nitric oxide synthesis isoforms (nNOS, iNOS, and eNOS) in thoracic spinal cord segments and nodose ganglia of rats with gamma-irradiated livers. Male rats (n = 32) were divided into equal groups A, B, C, and D. In group A, the controls, no radiation was applied, while groups B, C, and D received 10 Gy of ionising gamma radiation. The rats of group B were euthanized at the end of the first day (d1), those of group C on the second day (d2), and those of group D on the third day (d3). The liver, spinal cord segments, and nodose ganglion tissues were dissected and fixed, and the liver sections were examined histopathologically. The other tissues were observed through a light microscope. Regeneration occurred at the end of d3 in hepatocytes which were radiation-damaged at the end of d1 and d2. On d1, some nNOS-positive staining was found in the neuronal cells of laminae I–III of the spinal cord and in neurons of the nodose ganglion, and on d3, some staining was observed in lamina X of the spinal cord, while none of note was in the nodose ganglion. Dense iNOS-positive staining was seen on d1 in the ependymal cells of the spinal cord and in the glial cells of the nodose ganglion, and on d3, there was still considerable iNOS staining in both tissues. There was clear eNOS-positive staining in the capillary endothelial cells of the spinal cord and light diffuse cytoplasmic staining in the neurons of the nodose ganglion on d1, and on d3, intense eNOS-positive staining was visible in several endothelial cells of the spinal cord, while light nuclear staining was recognised in the neurons of the nodose ganglion. The nNOS, iNOS, and eNOS isoforms are activated in the spinal cord and nodose ganglion of rats after ionising radiation insult to the liver.

Sublethal irradiation of BALB/c mice 4 hours prior to inoculation with 5 X 10(4) virulent Brucella abortus, caused significant (P < 0.01) reductions in bacterial numbers in comparison with numbers in unirradiated controls. Numbers of brucellae in the spleen were significantly lower by 5 days after inoculation and decreased thereafter, so that at 2 and 3 weeks after inoculation, there were up to 1,000-fold fewer organisms in the spleen of irradiated mice. The number of brucellae in the spleen increased in irradiated mice thereafter. The course of events in the liver was similar, but developed more slowly, and peak differences in bacterial numbers were about 1 log less. These phenomena were not attributable to differences in implantation of brucellae in the liver or spleen, nor to an abnormal distribution of organisms in other organs of irradiated mice. Irradiation of mice during the plateau phase of infection also resulted in significant (P < 0.05) reductions in bacterial counts in the spleen during the succeeding 4 weeks. Macrophage activation in the spleen, measured by a Listeria monocytogenes-killing assay, was significantly (P < 0.01) increased by irradiation alone at 1 week after inoculation and at that time was significantly (P < 0.01) greater in B abortus-infected, irradiated mice than in B abortus-infected controls. Histologic, cytologic, and immunologic studies revealed that the decrease in numbers of organisms between 1 and 2 weeks after inoculation in irradiated mice occurred at a time when their immune response to B abortus was suppressed and when numbers of neutrophils and monocytes infiltrating the spleen were significantly (P < 0.01) diminished. The increase in numbers of B abortus in organs of irradiated mice that began after the third week coincided with recovery of the immune response and an increase in numbers of neutrophils and monocytes in the infected organs. The course of B abortus infection was not substantially altered during the first 11 days after inoculation in mice infected at the height of a profound monocytopenia and neutropenia induced by azathioprine, a drug that by itself failed to activate macrophages. We hypothesized that, in irradiated mice, a rapid radiation-induced activation of resident macrophages to a brucellacidal state was coupled with an absence of newly formed monocytes in which virulent strains of B abortus could establish persistent infection, and that as susceptible monocytes emerged in mice recovering from the effects of irradiation, chronic infection became established.

The purpose of the study was to verify the existence and pathogenicity of Aeromonas hydrophila (A. hydrophila) in fish by validating the bactericidal effects of microwave and Gamma radiation on infected fish fillets. A total of 100 frozen Basa fish fillet samples were collected randomly from different markets in Zagazig, Sharkia Governorate, Egypt, and subjected to microbiological examination. The results revealed a 14% prevalence rate of A. hydrophila in fish fillets, which were tested for the presence of seven virulence genes: aerA, act, ast, alt, hyl, ahhR, and ahh1. All isolates exhibited traits related to virulence. The most predominated gene was ast (64.2%), followed by aerA, act, hyl, and ahhR (57.14% for each). Then, an experimental protocol for several treatments showed that Gamma radiation at a dose of 1 kGy decreased the count of A. hydrophila in fish fillets by 4.4 log10 CFU/g whereas doses of 2 and 3 kGy eradicated the pathogen. The same positive effect was recorded towards the microwave after cooking for 1, 2, and 3 minutes. Therefore, using microwave cooking and Gamma-irradiation alone and in combination with other decontamination methods may be more efficient in lowering the pathogen counts in fish meat.

Aflatoxins are one of the most dangerous toxic residues in various foods including poultry. This study was conducted to assess the reducing effect of gamma radiation on the levels of aflatoxin B1 in poultry meat, skin, and liver. To this end, a total of 80 poultry samples including meat, skin, and liver were surveyed for the incidence of aflatoxins, where only positive samples (27 samples of muscle, skin, and liver; 9 samples each) were selected for testing the effect of treatment by gamma radiation. The levels of aflatoxins were estimated in the examined samples using High Performance Liquid Chromatography (HPLC) whereas positive samples were exposed to 0 kGy, 5 kGy, or 10 kGy, and the differences in aflatoxin contents before and after exposure were calculated. The obtained results clarified that radiation achieved reduction rates in aflatoxin B1 level in muscle samples with a mean value 99.259±0.741, and 100.00±0.00% when treated with 5 kGy and 10 kGy, respectively. Whereas in skin samples, 98.676±1.324 and 100.00±0.00 % when treated 5 kGy and 10 kGy, respectively. While in liver samples, reduction rates accounted for 84.312±7.406 and 88.249±10.882 were obtained when treated with 5 kGy and 10 kGy, respectively. In conclusion, the exposure of poultry meat, skin, and liver to gamma radiation (5kGy or 10 kGy) has a significant reducing effect (p<0.05) in aflatoxins B1. The results were discussed from the hygienic point of view and compared with the national and international standards to assess their reliability for consumption.