Page 72 - VERITAS Vol.2 Issue 2
P. 72

A REVIEW ON FREQUENCY



                 AND PREVALENCE OF PYRE-



              THROID POISONING IN INDIA



        Veritas Volume: 2, Issue: 2, Pages:63-69
                                                                     Ms. Riya Raj C A


        INTRODUCTION

        Poisoning is one of the most ancient crimes among humanity and

        one that will never fade in society. The intentions of poisoning range

        from accidental, homicidal, to suicidal. The choice of poisons also

        differ across intentions of poisoning. For example, a suicidal poison
        choice would be an easily available, yet effective poison, whereas an

        accidental or homicidal poison may go unnoticed (less effective) for

        many days. Traditional pesticides are the organophosphates, organo-

        chlorines, and carbamates that are commonly used in pest manage-

        ment in the agro-business. A new and emerging class of pesticides

        are the pyrethroids which are of interest in forensic science due to its

        undue use in poisoning - both with suicidal and homicidal intent.
        Pyrethroids are a synthetic version of pyrethrin, a naturally occurring

        pesticide found in chrysanthemum (flower). They were developed in

        such a way as to maximise their stability in the environment. It has in-

        secticidal properties of pyrethrin that are strongly lipophilic and rap-

        idly penetrate into insects, paralysing their nervous system.

        In this background, some facts about pyrethroids are presented below:

        Chemistry of pyrethroids -  Pyrethrins are a mixture of six structurally
        related insecticidal esters formed by a combination of two acids (chry-

        santhemic acid and pyrethric acid) and three alcohols (pyrethrolone,

        cinerolone, and jasmolone). The mode of action of pyrethroid poison-

        ing - They act as axonic excitotoxins, i.e., the toxic effects are medi-

        ated by preventing the closure of the voltage-gated sodium channels

        in the axonal membranes. When the toxin keeps the channels in their

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