Cypermethrin and beta-cyfl uthrin are two most widely used multipurpose pyrethroids. After determining their oral LD 50 (416.98 mg kg -1 and 354.8 mg kg -1 body weight, respectively), we assessed their hepatotoxicity in Wistar rats following acute (0.1 LD 50 for 1 day) and sub-acute (0.1 LD 50 for 7, 14, 21 or 28 days) poisoning. The assessment was based on hepatic marker enzymes AST, ALT, LDH, ALP, glycogen, total proteins, total lipids, cholesterol, free fatty acids, and phospholipids. AST, ALT, LDH, total lipids, cholesterol, phospholipids, and free fatty acids in hepatic homogenate increased following pyrethroid stress. In contrast, hepatic proteins, glycogen, and ALP activity decreased due to lysis of structural proteins and leakage of enzymes into the blood stream. Biochemical data were consistent with histological alterations (cytoplasmic vacuolisation, nuclear polymorphism, eccentric nucleus, karyolysis, karyorrhexis, and sinusoidal dilation). Comparatively greater hepatocellular damage was noted in beta-cyfl uthrin than in cypermethrin-treated rats, which is probably related to the fl uorine atom in beta-cyfl uthrin.

Present study was aimed to evaluate the median lethal dose (LD50) of two broadly used, type II pyrethroid pesticides Cypermethrin and Beta-cyfluthrin against Wistar albino rats. The albino rats corresponding to experimental sets were orally administrated different doses of selected pyrethroids for estimation of median lethal dose. LD50 has been calculated by Log-dose/probit regression line method, and came out to be 416.98 and 354.8 mg/Kg b.wt. for Cypermethrin and Betacyfluthrin respectively. Difference in the median lethal of these compounds may be a consequence of structural differences

Pesticides are the main remedy for pest eradication, but their use has been found to be harmful also to various non-target organisms. In this study, giant cell formation was observed in hepatocytes of experimental albino rats following two type II pyrethroid pesticdes, Cypermethrin and Beta-cyfluthrin. Histopathological examination was done for this purpose and the results revealed the formation of giant cells and polyploidy condition following intoxication of these experimental compounds with Beta-cyfluthrin, with an edge over, and Cypermethrin, probably due to structural differences.

Pyrethroids, commercially available pesticides, are greatly in use these days, and thus they carry considerable chances of contaminating various ecosystems. Haematotoxicity of cypermethrin, a broadly used type II pyrethroid, has been assessed in the present study. Selected parameters included determination of total RBC count, haemoglobin concentration (Hb conc.), packed cell volume (PCV), mean corpuscular volume (MCV), mean corpuscular haemoglobin (MCH), mean corpuscular haemoglobin concentration (MCHC), erythrocyte sedimentation rate (ESR), total leukocyte count (TLC), differential leukocyte count (DLC), along with qualitative analysis of blood and bone marrow. Of these parameters, those showing significant decline following cypermethrin intoxication included total RBC count, Hb conc., PCV, MCV, MCH, whereas non-significant decrease was observed in the case of MCHC. ESR, TLC and DLC, on the other hand, increased significantly following cypermethrin intoxication. Qualitative changes included altered red cell morphology such as microcystosis, appearance of stomatocytes, poikilocytosis, giant platelet formation, etc. in peripheral blood and increased erythroid precursors in bone marrow of treated rats. These parameters were however normalised following twenty-two days of recovery phase.

The toxicity of various forms of mercury to the living organisms is well documented. Mammalian kidney is the main site of decomposition of inorganic mercury as well as the target organ for its toxicity in majority of the animals including human beings. Present study has been aimed to investigate the role of Tageteserecta(family-Astereacea) as a possible modifier of mercury induced renal damages. Experimentation was conducted on one hundred female albino rats, divided into five equal groups, each group again sub-divided into four sub-groups having five rats each: Control group- Orally administrated distilled water only. T. erecta flower extract treated group-10mg/kg b. wt./day for 1, 7, 14, 21 days was administrated orally. Mercuric chloride treatment groups-A dose of 0.926 mg/kg b.wt. for 01 day, 0.132 mg/kg b.wt. for 7 days, 0.066 mg/kg b.wt. for 14 days and 0.044 for 21 days was administrated through oral route. Oral administration of T. erecta flower extract followed by mercuric chloride treatment for 1, 7, 14 and 21 days. Oral administration of Mercuric chloride followed by T. erectaflower extractadministration for 1, 7, 14 and 21 days. These animals were then sacrificed after 1, 7, 14 and 21 days treatment respectively. Controls were also run respectively. Mercuric chloride intoxication resulted in pathological alterations in the kidney of albino rats, such as degradation of glomerulus, proximal and distal tubules. Combined pre and post treatment of T. erectawith mercuric chloride has been found to reduce the pathological alterations in the kidney. Thus, the results from the present study suggest that T. erectacan modify the renal damages against mercuric chloride induced toxicity.