Potential toxic effects of diethnolamine on the nervous system of adult albino rats

الملخص EN

Background/Aim : diethndamine (DEA) is widely used in the preparations of cosmetics, shampoos, hair conditioners and skin cleaners Many pharmaceutical drugs and pesticides contained DEA as a solubilizing or dispersing agent.

The wide consumption of DEA all over the world and the limited information available on its health effects provoked this experimental research to evaluate the toxic effect of DEA as an indicator of the hazardous effects on the nervous system.

Materials &Methods: The study was conducted on72 adult male albino rats, divided into two major groups (36 rats each) according to the routes of exposure to DEA (dermal and oral).

Each group was divided into two groups according to duration of exposure (2 weeks and 13 weeks).

Each was then subdivided into control and 3 DEA exposed groups according to the dose of DEA.

The cerebellum and the cervical spinal cord were extracted and fixed in 10 % buffered formalin for histological examination Results : hypo activity was observed in all the rats exposed to DEA for 2 weeks (either dermal or oral) where hypoactive city and Consul so ns o occurred i n prolog needed poser e (13 w eek).

Mortal! Try rate was s higher in oral than in dermal application and death was preceded by convulsions.

As regards the cerebellum ; after 2weeks of dermal application of DEA, there were shrunken Purkinje cells and vacuolated molecular layer.

Long term application (13 weeks) of high doses caused marked degeneration of the Purkinje cell layer and clumped cells of the granular layer.

Oral administration for 2 weeks caused marked dose dependent degeneration of the Purkinje cell layer, high dose (10,000 ppm / kg), caused severe damage with small or large coalescent spaces in the three layers of the cerebellum.

Oral administration of small dose of DEA for 13 weeks caused degeneration of some Purkinje cells whereas high dose (5000 ppm / kg) caused foci of necrosis and loss of nervous tissues in the granular and molecular layers in addition to the degeneration of the Purkinje cells.

As regards the ventral horn of the cervical spiral cord; dermal application of DEA for 2 weeks caused degeneration of the nerve cells art! Vacuolated interstitial whereas its dermal application for 13 weeks caused dos e dependent progress! Vet atrophy of the anterior torn nerve cells.

Higher doses (500 mg / kg) caused massive destruction of nerve cells with areas of necrosis.

Oral administration for 2 weeks caused a dose dependent degeneration of the nerve cells.

High dose (10000 ppm / kg) caused large areas of necrosis and degenerated nerve cells Oral administration for 13 weeks caused progressive atrophy of the nerve cells.

High doses of DEA (5000 ppm/kg) for 13 weeks caused marked replacement of the grey matter by glial tissues with spotty hemorrhage and congested blood vessels.