Exposure to Di-n-butyl Phthalate Causes Modulation in Neurotransmitter System of Wistar Rats: A Multigenerational Assessment.

Neuroendocrine regulation is disrupted by di-n-butyl phthalate (DBP) when exposure occurs during the critical periods of fetal development, which can lead to neurological disorders. To evaluate the toxic potential of DBP, it is necessary to conduct teratological studies, which could determine impacts on the development of the fetus. The present study was designed to understand the sequelae of neuroendocrine regulation in one-month-old pups when rats were exposed to DBP (F-F) and during lactation.

Genotoxic impact of di-n-butyl phthalate on DNA: A comparative study of three generations in the neuronal tissue of Wistar rats.

Di-n-butyl phthalate (DBP), one of the plasticizers, is considered a ubiquitous environmental contaminant due to its widespread application in personal-care products and serves as a raw material in many industries for the generation of many plastic products. Several scientific investigations have shown that DBP caused embryotoxicity and cognitive impairments. However, there is less understanding of the genotoxic potential of DBP in neuronal tissue when exposure happens continuously for several generations.

Neuroprotective Actions of Clinoptilolite and Ethylenediaminetetraacetic Acid Against Lead-induced Toxicity in Mice Mus musculus.

Objectives: Oxidative stress is considered as a possible molecular mechanism involved in lead (Pb(2+)) neurotoxicity. Very few studies have been investigated on the occurrence of oxidative stress in developing animals due to Pb(2+) exposure. Considering the vulnerability of the developing brain to Pb(2+), this study was carried out to investigate the effects of Pb(2+) exposure in brain regions especially on antioxidant enzyme activities along with ameliorative effects of ethylenediaminetetraacetic acid (EDTA) and clinoptilolite.

Influence of fluoride on streptozotocin induced diabetic nephrotoxicity in mice: protective role of Asian ginseng (Panax ginseng) & banaba (Lagerstroemia speciosa) on mitochondrial oxidative stress.

Background & Objectives: Chronic fluoride intoxication through drinking water is a serious health problem. Patients with diabetes are known to have impaired renal function and elimination of fluoride from the body is mainly done through kidney. Fluoride toxicity in diabetes patients may aggravate complications.

Chronic fluoride toxicity and myocardial damage: antioxidant offered protection in second generation rats.

This experiment was designed to investigate the extent of peroxidative changes and histological alterations in the myocardium of rats exposed to high fluoride for two generations, in addition to ameliorative role of selenium and vitamin E on the above indices. Adult albino Wistar rats were given fluoride through drinking water (200 ppm F) and maintained subsequently for two generations, while they were exposed to fluoride throughout the experiment. Fluoride treatment significantly increased the lipid peroxidation and decreased the activity of antioxidant enzymes, viz.