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Anand Agricultural University, Anand

Anand Agricultural University (AAU) was established in 2004 at Anand with the support of the Government of Gujarat, Act No.(Guj 5 of 2004) dated April 29, 2004. Caved out of the erstwhile Gujarat Agricultural University (GAU), the dream institution of Sardar Vallabhbhai Patel and Dr. K. M. Munshi, the AAU was set up to provide support to the farming community in three facets namely education, research and extension activities in Agriculture, Horticulture Engineering, product Processing and Home Science. At present there seven Colleges, seventeen Research Centers and six Extension Education Institute working in nine districts of Gujarat namely Ahmedabad, Anand, Dahod, Kheda, Panchmahal, Vadodara, Mahisagar, Botad and Chhotaudepur AAU's activities have expanded to span newer commodity sectors such as soil health card, bio-diesel, medicinal plants apart from the mandatory ones like rice, maize, tobacco, vegetable crops, fruit crops, forage crops, animal breeding, nutrition and dairy products etc. the core of AAU's operating philosophy however, continues to create the partnership between the rural people and committed academic as the basic for sustainable rural development. In pursuing its various programmes AAU's overall mission is to promote sustainable growth and economic independence in rural society. AAU aims to do this through education, research and extension education. Thus, AAU works towards the empowerment of the farmers.

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20121
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Subject: Veterinary Pharmacology and Toxicology × Author: SINHA, SUPRITA × End date: 2020 × Start date: 2010 × Thesis Type: Ph.D ×
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    ThesisItemOpen Access
    STUDIES ON LEAD ACETATE AND THIAMETHOXAM INDUCED IMMUNOTOXICITY AND GENOTOXICITY AND EVALUATING THE AMELIORATING POTENTIAL OF TINOSPOARA CORDIFOLIA IN MICE
    (AAU, Anand, 2012) SINHA, SUPRITA; Thaker, A. M.
    The present study was conducted on healthy albino mice of about 4-5 weeks of age. All mice were randomly divided into thirteen groups (group I to XIII) each containing 6 mice. Lead acetate was administered by dissolving in drinking water whereas, other treatment of thiamethoxam and aqueous extract of Tinospora cordifolia were given once daily orally with 1 ml BD syringe, for 28 days. The first two groups of mice i.e. group I and II were administered 1/10th (87.1 mg/kg) and 1/20th (43.5 mg/kg) of LD50 of thiamethoxam (871 mg/kg b.w.) suspended in com oil daily for 28 days. Group III was administered lead acetate @ 15 mg/kg dissolved in drinking water. Group IV and V mice received combination of lead acetate (15 mg/kg) and 1/10th (87.1 mg/kg) and 1/20th (43.5 mg/kg) of LD50 of thiamethoxam. Groups VI and VII were administered aqueous extract of Tinospora cordifolia (100mg/kg) and 1/10th (87.1 mg/kg) and 1/20th (43.5 mg/kg) of LD50 of thiamethoxam respectively. Group VIII was given lead acetate (15 mg/kg) and Tinospora cordifolia extract (100 mg/kg). Groups IX and X were administered 1/10th (87.1 mg/kg) and 1/20th (43.5 mg/kg) of LD50 of thiamethoxam respectively along with lead acetate (15 mg/kg) and Tinospora cordifolia extract (100 mg/kg). Groups XI and XII were kept as negative control and were gavaged with Tinospora cordifolia extract (100 mg/kg) and com oil (1 ml) orally respectively. Group XIII served as a positive control group and was given cyclophosphamide (20 mg/kg) for genotoxicity study following intra peritoneal administration 24 hours prior to sacrifice i.e. on 27th day of experiment. Ail the mice were monitored for any observable toxic symptoms throughout the experiment period and they were also weighed weekly to monitor gain in body weight. Before sacrifice, the blood samples were collected and analyzed for hematological, biochemical, immunological and genotoxic parameters. After scarifice, bone marrow from femur was collected for both micronuclei and chromosomal aberration tests. There were noticeable signs and symptoms like pawing, burrowing and tremors in the treated animals. Severity of symptoms was high in animals given high dose of thiamethoxam. During the last quarter of the experiment, animals appeared dull, depressed and anorectic in the treated groups (given lead acetate and thiamethoxam). However, there was no mortality at both the dose levels of thiamethoxam and lead acetate. Significant decrease in body weight gain of the thiamethoxam and lead acetate treated mice as compared to control group was observed. Thiamethoxam, at high and low dose levels (87.1, 43.5 mg/kg b.w.) was found to be non-genotoxic as it produced non-significant change in chromosomal aberrated cells, micronuclei formation and non significant damage to DNA integrity in comet assay. Lead acetate, at the dose rate of 15 mg/kg b.w. showed significant increase in micronuclei, chromosomal aberrated cells and percentage of comet cells. There was no augmentation of genotoxic effect in the group treated with combination of lead acetate and thiamethoxam.