Determination of genoprotection against cyclophosphamide induced toxicity in bone marrow of Swiss albino mice by Moringa oleifera leaves and Tinospora cordifolia stem.

The present study aimed to determine the genoprotective activity and safety of Moringa oleifera leave and Tinospora cordifolia stem extracts against cyclophosphamide (CP)-induced genotoxicity utilizing Swiss albino mice. Animals were divided into 14 groups for subacute treatment with either M. oleifera or T. cordifolia extracts daily for 28 days. The extract doses selected were 100, 200 or 400 mg/kg b.w administered orally alone or combined with CP (50 mg/kg b.w. intraperitoneally daily for 5 days). Analyses performed included the comet assay, micronucleus test (MN) in bone marrow cells and sperm head abnormality assay (SHA). M. oleifera and T. cordifolia extracts induced no significant genotoxic effects on somatic and germ cells. In contrast, for all cells examined M. oleifera and T. cordifolia extracts inhibited DNA damage initiated by CP. Taken together data demonstrated that both plant extracts did not exhibit marked genotoxic effects but displayed potential chemoprotective properties against CP-induced genotoxicity in Swiss mice.

Immunopathological studies on Escherichia coli infected broiler chickens fed on Aloe vera leaf extract.

Escherichia coli infection is the major bacterial disease affecting the poultry industry and the continuous use of antibiotics in poultry farming has resulted in antibiotic resistance. So this study was planned to evaluate the use of an ecologically safe alternative to fight against infections. The leaf gel of the Aloe vera plant was selected based on its antibacterial activity assessed in in-vitro tests. The objective of the present study was to evaluate the effect of A. vera leaf extract supplementation on the severity of clinical signs and pathological lesions, mortality rate, levels of antioxidant enzymes, and immune response in experimentally E. coli-infected broiler chicks. Broiler chicks were supplemented with aqueous Aloe vera Leaf (AVL) extract @ 20 ml per liter of water from day one of age. After seven days of age, they were experimentally infected with E. coli O78 @ 107 CFU/0.5 ml intraperitoneally. Blood was collected at weekly intervals up to 28 days and assayed for antioxidant enzyme assays, and humoral and cellular immune response. The birds were observed daily for clinical signs and mortality. Dead birds were examined for gross lesions and representative tissues were processed for histopathology. The activities of antioxidants, Glutathione reductase (GR), and Glutathione-S-Transferase (GST) were significantly higher than the control infected group. The E. coli-specific antibody titer and Lymphocyte stimulation Index were comparatively higher in the AVL extract-supplemented infected group as compared to the control infected group. No considerable change was noted in the severity of clinical signs and pathological lesions, and mortality. Thus, Aloe vera Leaf gel extract enhanced the antioxidant activities and cellular immune responses of infected broiler chicks to combat this infection.

Assessment of anilofos-induced mutagenicity in bone marrow and germ cells of Swiss albino mice.

Anilofos is an organophosphate compound and is used extensively as a preemergence and early postemergence herbicide for the management of sedges, annual grasses, and some broad-leaved weeds in rice fields. The present study was aimed to assess the mutagenic potential of anilofos after sub-chronic exposure in Swiss albino mice. For this, a combined approach employing micronucleus (MN), chromosomal aberration (CA) studies and sperm-head abnormalities (SHAs) was used. Three dose levels of 1%, 2%, and 4% of maximum tolerated dose (MTD) (235 mg/kg b.wt.), that is, 2.35, 4.7 and 9.4 mg/kg b.wt., respectively, were administered orally daily for 90 days. A higher incidence of micronucleated erythrocytes (polychromatic erythrocytes + normochromatic erythrocytes), significant increase in CA frequency, and significant decrease in the ratio of polychromatic/normochromatic erythrocytes (P/N) ratio were observed at the 4.7 and 9.4 mg/kg b.wt. dose levels. A significant increase in SHA was observed in all treatment groups (2.35, 4.7, and 9.4 mg/kg b.wt.) from the control group. In conclusion, anilofos exposure of 2% and 4% of MTD caused a higher rate of micronucleated erythrocytes, increased frequency of CA, increase in SHA, and lower P/N ratio, and pesticide exposure of 1% of MTD only resulted in higher SHAs. Thus, anilofos was found to have mutagenic potential in mice when administered daily orally at dose rate of 4.7 and 9.4 mg/kg b.wt. for 90 days.

Ameliorating effect of Withania somnifera root extract in Escherichia coli-infected broilers.

The present study was undertaken to investigate the effect of aqueous Withania somnifera root (WSR) extract in broiler chicks experimentally infected with Escherichia coli O78 @ 107 CFU/0.5 ml intraperitoneally. Clinical signs and mortality due to colibacillosis observed in infected chicks were mild and lasted for short duration in WSR extract supplemented group as compared with the nonsupplemented group. A significant increase in serum alanine transaminase, aspartate transaminase, lactate dehydrogenase, and creatine phosphokinase activities and a decrease in total protein and albumin concentrations were observed in the infected groups, though these changes were of lower magnitude in WSR extract supplemented group. A significantly higher activity of oxidative blood parameters such as superoxide dismutase, catalase, glutathione reductase, and glutathione-S-transferase enzymes were noticed in WSR extract supplemented group. The WSR extract supplemented group revealed significantly higher E. coli-specific antibody titer and enhanced lymphocyte proliferation response as compared with the nonsupplemented group. The gross and histopathological lesions of colibacillosis were mild in the WSR extract-supplemented infected group as compared with the nonsupplemented infected group. Withania somnifera root extract supplementation produced 31.48 and 34.38% protection in the gross and histopathological lesions in E. coli infected chicks, respectively. It is concluded that supplementation of 20% WSR extract @ 20 ml/L of water caused a reduction in the severity, mortality, and recovery period of E. coli infection and enhanced the humoral and cellular immune responses suggesting its protective effect on limiting the pathology of E. coli infection in broiler chickens.

Assessment of acetamiprid-induced genotoxic effects in bone marrow cells of Swiss albino male mice.

Acetamiprid (ACE), a neonicotinoid insecticide, is widely used in agriculture either alone or in combination with other insecticides. A combined approach employing micronucleus test (MNT) and chromosomal aberrations (CA) assay was utilized to assess the genotoxic effects of ACE in bone marrow of Swiss albino male mice. Acetamiprid was administered i.p. daily at 4.6 and 2.3 mg/kg/day along with 3% gum acacia as negative control for 60 and 90 days and cyclophosphamide (50 mg/kg b.wt.) as positive control. ACE treatment resulted in a dose-dependent increase in the frequencies of micronuclei per cell and chromosomal aberrations in bone marrow cells. The increased micronuclei formation in total erythrocyte cells (immature PCEs and mature NCEs) was observed only at higher dose level (4.6 mg/kg b.wt.) administered for 90 days. The test also indicated the cytotoxic effect of higher dose level of pesticide by PCE/NCE ratio. The number of chromosomal aberrations were increased in the pesticide treated group compared to the negative control group, although significant increase was observed only in the group exposed to higher dose level of pesticide for both 60 and 90 days. Thus, daily exposure of ACE at a dose level of 4.6 mg/kg body weight for 60 and 90 days caused genotoxic and cytotoxic effects on the somatic cells of Swiss albino male mice.

Assessment of imidacloprid-induced mutagenic effects in somatic cells of Swiss albino male mice.

Pesticides are being used for plant protection to increase food protection and to reduce insect-borne diseases worldwide. Exposure to the pesticides may cause genotoxic effects on both the target and nontarget organisms, including man. Therefore, the mutagenicity evaluation of such pesticides has become a priority area of research. Imidacloprid (IMI), a neonicotinoid insecticide, is widely used in agriculture either alone or in combination with other insecticides. A combined approach employing micronucleus test (MNT) and chromosomal aberrations assay (CA) was utilized to assess the mutagenicity of imidacloprid in bone marrow of Swiss albino male mice. IMI suspension was prepared in 3% gum acacia and administered at doses of 5.5, 11 and 22 mg/kg body weight for 7, 14 and 28 days to mice. IMI treatment resulted in a dose and time-dependant increase in the frequencies of micronuclei per cell and chromosomal aberrations in bone marrow cells. A statistically significant increase in chromosomal aberrations and micronuclei/cell was found only after daily treatment of IMI at highest selected dose (22 mg/kg body weight) for longest selected time period (28 days) compared to the control group. Thus, daily exposure of imidacloprid at a dose level of 22 mg/kg body weight for 28 days caused mutagenic effects on the somatic cells of Swiss albino male mice.

An in vivo assay of the mutagenic potential of imidacloprid using sperm head abnormality test and dominant lethal test.

OBJECTIVE: To assess the mutagenic effects of imidacloprid in germ cells of Swiss albino male mice by sperm head abnormality (SHA) assay and dominant lethal test (DLT). METHODS: Swiss albino mice were exposed to imidacloprid (22, 11 and 5.5 mg/kg/day) along with 3% gum acacia as vehicle control through oral route for 7, 14 and 28 days for SHA assay and for 28 days for DLT. The epididymal sperm smear in 1% eosin stain was analyzed for SHAs. In DLT, male mice were allowed to mate with females after 1, 3 and 6 weeks of end of pesticide treatment. The uterine contents of the sacrificed females were observed for live and dead implants. The analysis of test and control groups data was done by one way ANOVA at p < 0.05. RESULTS: Exposure of all dose levels of imidacloprid (22, 11 and 5.5 mg/kg/day) for seven days did not induce significant SHAs while they induced significant SHAs compared with the control group following exposure for 14 and 28 days. The analysis of uterine content revealed a significant increase in the number of dead implants/female compared with the vehicle control in only those females which were mated with male mice after six weeks of treatment of highest dose level of imidacloprid. The dominant lethal mutations were observed only at spermatogonial stage. CONCLUSIONS: Long-term exposure of pesticide generated SHAs even at lowest dose level (5.5 mg/kg/day for 14 days) and mutagenic effects at spermatogonial stage at highest dose level (22 mg/kg/day for 28 days).