Objectives Thousands of food additives are being used by the food industries in ready to eat packed food. These food additives act as either preservatives or enhancers of palatability. Monosodium glutamate (MSG), a sodium salt of glutamic acid is a widely used food additive for enhancing taste. It gives the unique taste to the food called “Umami” or “Savory taste”, which is different from four primary tastes namely, sweet, sour, salty, and bitter. The current experimental study was investigated by dose-related effects of MSG on adult Wistar rats using histological and histomorphometric techniques. Methods Twenty-eight adult Wistar rats were divided into four groups i.e.; one control and three experimental groups. Rats were administered orally with different doses of MSG to the experimental groups and distilled water to the control groups consecutively for 45 days. At the end of the study, rats were sacrificed and tissues were collected for the examination. Results Histomorphometric data of the nuclei diameter of hepatocytes showed significant variation between control and experimental groups. Less PAS-positive material found in a higher dose of MSG-induced rats in histochemical observation. Conclusions One of the challenges of the problem of animal experimental studies is the application of results to human dietary intake of MSG. Based on the dose-dependent findings of the current study; it is evident that the administration of MSG is hepatotoxic in adult Wistar rats.

This study was done to show the changes in the liver following diclofenac treatment and to study the hepatoprotective effects of Vitamin E and A in diclofenac treated rats. Rats were divided into four groups of six rats each. Group-1: Control rats (n= 6), Group-2: Rats (n= 6) treated with diclofenac at dose of 50 mg/kg IM for 7 days, Group-3: Rats (n= 6) treated with Vitamin A at dose of 400 IU/kg orally followed by diclofenac at 50 mg/kg IM 2 h later for 7 days, and Group 4: Rats (n= 6) treated with Vitamin E at dose of 200 IU/kg orally followed by diclofenac at 50 mg/kg IM 2 h later for 7 days. Later it was analysed with standard biomarkers, and it was histologically interpreted. The results showed that there was an rapid increase in the levels of liver function test in diclofenac treated group, which was significantly decreased after pre-treatment with vitamin E than vitamin A. The liver acinus showed centriacinar necrosis of hepatocytes after 7 days of diclofenac treatment, which was prevented by administration of Vitamin E and A. Drug-induced liver injury possesses a major clinical problem and has become a leading cause of acute liver failure and transplantation. Overstressed liver compromises its detoxification role which may expose it to a variety of diseases and disorders. Diclofenac sodium is a phenylacetic acid derivative, a widely used nonsteroidal anti-inflammatory drug (NSAID) for the treatment of inflammatory conditions such as osteoarthritis, rheumatoid arthritis, polymyositis, dermatomyositis, dental pain and spondyloarthritis. Although the exact mechanism by which diclofenac injuries in liver is not understood, some studies explain the toxicity by affecting cytochrome P 450 leading to the production of active metabolites. Hepatoprotective effects of Vitamin E were better compared to Vitamin A following treatment with NSAIDS. Hence, it may be necessary to administer Vitamin E in patients treated with diclofenac.

Drug induced liver injury possesses a major clinical problem and has become leading cause of acute liver failure and transplantation. Overstressed liver compromises its detoxification role which may expose it to a variety of diseases and disorders. The present study was to determine whether pre- administration of various doses of vitamin E would have protective effect against diclofenac induced hepatotoxicity in wistar male rats. Twenty-four albino male rats weighing 180-200g were divided equally into four groups. In control group rats were administrated with physiological saline 2ml/kg b.wt /intramuscularly. Another group with 50mg/kg b.wt/ intramuscularly/seven days diclofenac was used for inducing toxicity. In experimental groups rats were administrated with different doses of vitamin E along with diclofenac sodium [200 and 400 IU orally and 50mg/kg b.wt/ intramuscularly/seven days]. Showed that there was a rapid increase in the levels of liver function test in diclofenac treated group, which was significantly decreased after pre-treatment with high dose than low dose of vitamin E. The liver acinus showed Centro acinar necrosis of hepatocytes after 7 days of diclofenac treatment, which was prevented by administration of Vitamin E. Drug-induced liver injury possesses a major clinical problem and has become a leading cause of acute liver failure and transplantation. Overstressed liver compromises its detoxification role which may expose it to a variety of diseases and disorders. Diclofenac sodium is a phenylacetic acid derivative, a widely used nonsteroidal anti-inflammatory drug (NSAID) for the treatment of inflammatory conditions such as osteoarthritis, rheumatoid arthritis, polymyositis, dermatomyositis, dental pain, spondyloarthritis, acute migraine, gout attacks and pain management in gall and renal stones. Although the exact mechanism by with diclofenac injuries liver is not understood, some studies explain the toxicity by affecting cytochrome P 450 leading to the production of active metabolites. Administration of different dose of diclofenac sodium induces severe adverse effects in liver and kidney.

Background Advanced maternal age is an important parameter associated with increased risk of feto-maternal complications and it is an evolving trend in society for women planning for pregnancy in late ages. However there are no studies done whether advanced maternal age has its effects on expression of growth pattern in the fetus. So this study was done to compare the maternal age with the third trimester fetal biometric parameters. Methods This study was done in 100 antenatal women and divided into two groups: Group 1: optimal maternal age group between 21–29 years of age and Group 2: advanced maternal age 30 and above. The pre-pregnant maternal weight, gestational age and third trimester fetal biometrics using ultrasound are noted and compared between the groups. Results The maternal weight gain between the groups was optimal but the third trimester fetal parameters were significantly less in advanced maternal age. The abdominal circumference in optimal age group and head circumference in advanced maternal age group was closer to calculated estimated date of delivery (EDD) and would be specific in calculating the gestational age. Conclusions Though there is no significant difference in maternal weight gain, there are fetal growth restrictions in advanced maternal age group due to which the third trimester fetal parameters are lesser than the optimal age group. Head circumference would be specific in calculating the estimated date of delivery in advanced maternal age group.