A comparative study on comprehensive nutritional profiling of indigenous non-bio-fortified and bio-fortified varieties and bio-fortified hybrids of pearl millets.

Seven indigenous pearl millet varieties, including non-bio-fortified (HC-10 & HC-20) and bio-fortified (Dhanashakti) and bio-fortified hybrids, viz., AHB-1200, HHB-299, HHB-311, and RHB-233, were studied in the present work. There was not any significant difference observed in the crucial anti-nutrients content, i.e., phytate (24.88-32.56 mg/g), tannin (3.07-4.35 mg/g), and oxalate (0.33-0.43 mg/g). Phytochemical content and antioxidant activity showed significantly high (p < 0.05) TPC and FRAP, TFC, and DPPH radical scavenging activity in the HHB 299 and Dhanashakti, respectively. Quantitative analysis of polyphenols by HPLC (first report on these varieties) revealed that HHB-299 has the highest amount of gallic acid. Fatty acid profiling by GC-FID showed that Dhanashakti, AHB-1200, and HHB-299 have rich monounsaturated fatty acid (MUFA) and polyunsaturated fatty acids (PUFA). Mineral analysis by ICP-OES showed high iron (87.79 and 84.26 mg/kg) and zinc (55.05 and 52.43 mg/kg) content in the HHB-311 and Dhanashakti, respectively. Results of the present study would help facilitate the formulation of various processed functional food products (RTC/RTE) that are currently not reported/unavailable. Supplementary Information: The online version contains supplementary material available at 10.1007/s13197-022-05452-x.

p53 Gene Mutation in Blood of Zebu Cattle with Squamous Cell Carcinoma of the Horn.

Horn cancer is one of the most important diseases in Zebu castrated male cattle. The objective of this study was to investigate the presence of p53 gene mutation in the blood of affected cattle and its value for early diagnosis and prognosis. The study was conducted on blood samples from 20 affected cattle and six healthy control cattle from Western India. Plasma samples were evaluated for the presence of p53 gene mutation using the polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) technique and the results were correlated with the stage of cancer. Five of the 20 cases had stage I neoplasms, nine stage II and six stage III, based on histopathological examination. PCR-SSCP analysis revealed an aberrant pattern of DNA migration on polyacrylamide gel electrophoresis of DNA extracts from blood samples of six animals with stage II and stage III cancer. No mutation was identified in blood from cattle with stage I cancer or from healthy control cattle. These results suggest that PCR-SSCP detection of p53 gene mutation in blood has potential diagnostic and prognostic value, and indicate the need for further large-scale investigation.

Clinico-haematological alterations and therapeutic management of tick borne fever in cross bred cow.

A 5 years old crossbred cow was brought to the Veterinary Clinical Complex of Lala Lajpat Rai University of Veterinary and Animal Sciences Hisar with history of progressive weakness, pale mucous membrane, anorexia, high fever (105 °F), tachycardia, laboured breathing and coffee coloured urine. Analysis of haematological parameters revealed severe anaemia, leucocytopenia, marked poikilocytosis of erythrocytes. Blood smear examination showed presence of signet ring shaped Theileria organisms, Babesia piroplasms and condensed dot forms of Anaplasma marginale in the stained erythrocytes. Further animal was treated with buparvaquone @ 2.5 mg/kg b.wt deep I/M in neck region and long acting oxytetracycline at 25 mg/kg b. W. slow I/V daily in normal saline solution for 5 days. Berenil (Diminazene aceturate 5%) injection was also administered @ 1 ml/20 kg b.wt. I/M along with supportive therapy. Clinical signs started to subside 3 days post treatment. Complete recovery was achieved by 4 weeks post treatment however animal succumbed to death due to immunosuppression.

Fipronil induced oxidative stress involves alterations in SOD1 and catalase gene expression in male mice liver: Protection by vitamins E and C.

In the present investigation, hepatic oxidative stress induced by fipronil was evaluated in male mice. We also investigated whether pretreatment with antioxidant vitamins E and C could protect mice against these effects. Several studies conducted in cell lines have shown fipronil as a potent oxidant; however, no information is available regarding its oxidative stress inducing potential in an animal model. Out of 8 mice groups, fipronil was administered to three groups at low, medium, and high dose based on its oral LD50 (2.5, 5, and 10 mg/kg). All three doses of fipronil caused a significant increase in the serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) level with concomitant increase in the absolute and relative weight of liver. High dose of fipronil caused significant down-regulation in the hepatic mRNA expression of superoxide dismutase 1 (SOD1) and catalase (0.412 ± 0.01 and 0.376 ± 0.05-fold, respectively) as well as an increase in the lipid peroxidation (LPO). Also, decrease in the activity of antioxidant enzymes; SOD, catalase, and glutathione-S-transferase (GST) and the content of nonantioxidant enzymes; glutathione and total thiol were recorded. Histopathological examination of liver revealed dose dependant changes such as severe fatty degeneration and vacuolation leading to hepatocellular necrosis. Prior administration of vitamin E or vitamin C against fipronil high dose caused decrease in lipid peroxidation and increased activity of antioxidant enzymes. Severe reduction observed in functional activities of antioxidant enzymes was aptly substantiated by down-regulation seen in their relative mRNA expression. Thus results of the present study imply that liver is an important target organ for fipronil and similar to in vitro reports, it induces oxidative stress in the mice liver, which in turn could be responsible for its hepatotoxic nature. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1147-1158, 2016.

Fipronil induced oxidative stress in kidney and brain of mice: protective effect of vitamin E and vitamin C.

Fipronil is a relatively new insecticide of the phenpyrazole group. Fipronil-induced effects on antioxidant system and oxidative stress biomarkers are yet to be studied in vivo. The present study was undertaken to evaluate fipronil-induced alterations in the blood biochemical markers and tissue antioxidant enzymes after oral exposure in mice and to explore possible protective effect of pre-treatment of antioxidant vitamins against these alterations. Mice were divided into eight groups containing control, test and amelioration groups. Mice in the test groups were exposed to different doses of fipronil, i.e., 2.5, 5 and 10 mg/kg bw, respectively for 28 days. Mice in the amelioration groups were treated with vitamin E or vitamin C (each at 100 mg/kg) 2 h prior to high dose (10 mg/kg) of fipronil. Fipronil exposure at three doses caused significant increase in the blood biochemical markers, lipid peroxidation and prominent histopathological alterations; while level of antioxidant enzymes was severely decreased both in kidney and brain tissues. Prior administration of vitamin E or vitamin C in the fipronil exposed mice led to decrease in lipid peroxidation and significant increase in activities of antioxidants, viz., glutathione, total thiol, superoxide dismutase and catalase. Vitamin E and vitamin C administration in fipronil exposed mice also improved histological architecture of the kidney and brain when compared with fipronil alone treated groups. Thus, results of the present study demonstrated that in vivo fipronil exposure induces oxidative stress and pre-treatment with vitamin E or C can protect mice against this oxidative insult.

Toxicopathological alterations induced by high dose dietary T-2 mycotoxin and its residue detection in Wistar rats.

T-2 toxin is one of the most potent cytotoxic and food-borne mycotoxins. Most experimental studies on the T-2 toxin have been performed at extremely low doses (ppb level). However, several field reports of contaminated feed have shown concentration of T-2 toxin to be as high as ≥20 ppm. Therefore, the impact of high dose T-2 toxin (20 ppm) after subacute exposure was investigated in an experimental setup with respect to growth performance, oxidative stress, and detailed pathomorphology in young male Wistar rats. Furthermore, to see the effect of such a high dose on the accumulation of T-2 toxin, its residues in various organs were quantified by high-performance thin-layer chromatography (HPTLC). Apart from obvious clinical toxicosis, rats in the toxin-fed group showed significant hemato-biochemical alterations and increased levels of biological markers of oxidative stress with concomitant decrease in levels of serum and tissue catalase and superoxide dismutase. These alterations were strongly supported by histopathological changes, such as hyperkeratosis and hyperplasia of the squamous gastric mucosa, oxidative damage to hepatocytes, atrophy of the thymus and spleen, and overall decrease in the spermatogenic activity of testes. An economical, simple, reliable, and quick method for the detection and quantification of T-2 toxin residues by HPTLC is also reported here. No residual T-2 toxin was detected in any of the organs tested, suggesting that T-2 toxin does not accumulate in tissues even at such a high exposure level.

Immunotoxic effects of imidacloprid following 28 days of oral exposure in BALB/c mice.

Imidacloprid, a neonicotinoid insecticide has been in use worldwide for several years in agriculture and veterinary medicine. It is possible that residue of this compound may be recycled in the food chain and thus information regarding effects from potential exposure to it is warranted. The objective of the present study was to evaluate immunotoxic effects of imidacloprid in female BALB/c mice. Imidacloprid was administered orally daily at 10, 5, or 2.5mg/kg over 28 days. Specific parameters of humoral and cellular immune response including hemagglutinating antibody (HA) titer to sheep red blood cells (SRBC; T-dependent antigen), delayed type hypersensitivity (DTH) response to SRBC, and T-lymphocyte proliferation in response to phytohemagglutinin (PHA) were evaluated. The results showed that imidacloprid at high dose, specifically suppressed cell-mediated immune response as was evident from decreased DTH response and decreased stimulation index of T-lymphocytes to PHA. At this dose, there were also prominent histopathological alterations in spleen and liver. Histopathological analysis of footpad sections of mice revealed dose-related suppression of DTH response. Imidacloprid at low dose of 2.5mg/kg/day did not produce any significant alterations in cellular and humoral immune response and it seemed to be an appropriate dose for assessment of 'no observable adverse effects level' for immunotoxicity in BALB/c mice. The results also indicated that imidacloprid has immunosuppressive effects at doses >5mg/kg, which could potentially be attributed to direct cytotoxic effects of IMD against T cells (particularly TH cells) and that long-term exposure could be detrimental to the immune system.