Pathology and molecular characterization of chicken infectious anemia virus and in silico antigen prediction.

The present study investigated five poultry flocks (size 142-600 birds) suspected of chicken infectious anemia (CIA) from Maharashtra, India. The necropsy of dead birds revealed severe atrophy of the thymus, gelatinization of bone marrow, subcutaneous hemorrhages, growth impairment, and severe anemia. Specific PCR targeting, 1390 bp fragment of the CIAV, VP1 gene was used in this study. Sequence analysis revealed that CIAV sequences of this study were grouped in genotype A. At the nucleotide level identity of 99.6% or more was seen between field sequences. At the amino acid level identity of 100% was seen between field sequences and NGP-1. Also, VP1 protein sequences of this study showed high identity with TJBD40, GD-K-12 strains from China and AB046590 strain from Japan. Further, the protein sequences of field CIAV had 0.7% to 2.5% divergence from VP1 sequences of vaccine strains. Antigenic epitopes of VP1 protein were predicted by SVMTriPtool and the field CIAV presented substitutions in two epitopes. To conclude, present study confirms the circulation of genotype A of CIAV in Maharashtra, India and predicted VP1 proteins of field CIAV revealed changes in two epitopes compared to vaccine strains.

Neurobehavioral alterations and histopathological changes in brain and spinal cord of rats intoxicated with acrylamide.

The aim of this project was to study the clinical manifestations, neurobehavioral, hematobiochemical, oxidative stress, genotoxicity, and histopathological changes during acrylamide toxicity in rats. A total of 30 adult male Wistar rats were divided in 5 equal groups and received 0, 10, 15, and 20 mg/kg body weight acrylamide as oral gavage, while group 5 was micronucleus (MN) control. Functional observational battery (FOB) parameters were studied at the 28th day of post treatment. Toxicological manifestations were evident in acrylamide-treated rats from 14th day onward. FOB revealed a significant change in central nervous system, neuromuscular, and autonomic domains. The hematological changes include significant decrease in concentration of hemoglobin, total erythrocyte count, packed cell volume, and mean corpuscular volume. The biochemical parameters aspartate aminotransferases, alkaline phosphatase, and albumin showed significant increase, while the levels of serum globulin and glucose were found to decrease significantly. The MN assay revealed the significant increase in frequencies of micronuclei and number of polychromatic erythrocytes. The oxidative stress parameters revealed no significant difference as compared to control rats. Histopathological changes observed in brain include neuronal degeneration, edema, and congestion, while spinal cord revealed demyelination in low-dose group and bilateral necrosis with malacia, liquefaction of white matter, and loss of myelin from gray matter in high-dose groups. The result indicates pathological alterations in brain and spinal cord and is responsible for neurobehavioral changes in rats. The FOB changes and histopathological alterations in spinal cord are in dose dependent to acrylamide intoxication. Various toxicological effects observed in experiment direct us to focus on a deep study and evaluate the possible causes pertaining to toxicity of this chemical. It would furnish the scientists with better options that would help them to search for a median path regarding the use of this chemical and take preventive measures to save the living beings from the hidden disasters of this chemical.

Evaluation of protective effect of vitamin e on acrylamide induced testicular toxicity in wister rats.

Male wistar rats (weighting 160-180 g) were divided in six groups of 6 animals per group. Group A and F served as control. Groups B, C, D and E received acrylamide at 20 mg/kg body weight for 28 days and groups C and E received additionally vitamin E (50 IU/kg body weight) for 1 to 28 days and 29 - 42(nd) days of experiment, respectively. The animals from groups A, B, and C were sacrificed on day 28(th) of experiment and from groups D, E, and F on 42(nd) day of experiment, respectively. There was significant decrease in the total sperm count and significant increase in the dead sperm count on day 28(th) of study due to acrylamide toxicity. At recovery period, there was significant increase in the total sperm count of vitamin-E-treated group of animals as compared to untreated toxicated rats. But, values were significantly lower than control animals. Microscopically, the lesions in the testes of acrylamide intoxicated rats at 28(th) day revealed destruction of seminiferous tubules at periphery. No spermatid and spermatocytes were seen in the seminiferous tubules. Detachment of spermatogonial cells started at periphery of seminiferous tubules. Atrophy of seminiferous tubules was a constant finding. Some tubules showed vacuolar degenerative changes in germinal epithelium. During the recovery period, destruction of seminiferous tubules, detachment of spermatogonial cells, and atrophy of seminiferous tubules were observed in group D and E. Few sections revealed only spermatogonial cells. At recovery period vitamin-E-treated rats revealed somewhat better architecture of the seminiferous tubules. Late spermatids were seen in few seminiferous tubules and other revealed starting of spermatogenesis. Thus, it appears that Vitamin E is not able to protect testes from acrylamide toxicity during active feeding, but after cessation of acrylamide feeding treatment with vitamin E revealed faster recovery as compare to not treated group.

Neuroprotective effect of vitamin e supplementation in wistar rat treated with acrylamide.

Male wistar rats (weighting 160-180 g) were divided into six groups of six animals per group. Groups A and F served as control. Groups B, C, D, and E received acrylamide at 20 mg/kg body weight for 28 days and groups C and E received additionally vitamin E (50 IU/kg body weight) for 1 to 28 days and 29 to 42 days of experiment, respectively. The animals from groups A, B, and C were sacrificed on day 28 of experiment and from groups D, E, and F on day 42 of experiment, respectively. The FOB (Functional Observational Battery) and histopathological changes were investigated at the end of 4(th) week and 6(th) week. FOB at the end of 4(th) week, of rats given acrylamide alone, or in combination with vitamin E, revealed a significant change in CNS, neuromuscular, and autonomic domains. A marked decrease in grip strength was recorded. A significant increase in foot splay, reduction in width and angle of sequential stride was noticed. Degenerative changes, necrosis, congestion, and kupffer cell proliferation in liver while vacuolar degenerative changes in tubular epithelium, coagulative necrosis, and hemorrhages in kidney were constant findings in acrylamide intoxicated rats. Neuronal degeneration, severe gliosis, congestion were found in brain. Spinal cord revealed demyelination. Acute microscopic softening of lumbar cord, bilateral necrosis with malacia and liquefaction of white matter, and loss of myelin from grey matter were seen. In the recovery period, vitamin E-treated rats revealed improvement in remyelination of spinal cord. In brain mild gliosis was seen. Thus, it appears that vitamin E is not able to protect them from acrylamide toxicity during active feeding, but after cessation of acrylamide feeding treatment with vitamin E revealed faster recovery as compared to the non-treated group.