Relative efficiency of Phyllanthus emblica fruit extract and ascorbic acid in modifying lead and aluminium-induced sister-chromatid exchanges in mouse bone marrow.

The identification of desmutagens and bioantimutagens in plants has prompted the search for additional plant extracts capable of modifying adverse cellular effects of environmental toxicants. The protective action of crude extracts of Phyllanthus emblica fruits (PFE) against lead (Pb) and aluminium (Al)-induced sister chromatid exchanges (SCEs) was studied in bone marrow cells of Mus musculus. The modifying effect of the crude extract was compared with that of comparable amounts of synthetic ascorbic acid (AA), a major component of the fruits. Oral administration of PFE or AA for 7 consecutive days before exposure of mice to the metals by intraperitoneal injections reduced the frequencies of SCEs induced by both metals. PFE afforded a more pronounced protective effect than AA in counteracting the genotoxicity induced by both Al and Pb: This difference was significant with Pb. The higher protection afforded by PFE may be attributed to the interaction of AA with other natural ingredients present in the crude fruit extract.

Modification of metal-induced micronuclei formation in mouse bone marrow erythrocytes by Phyllanthus fruit extract and ascorbic acid.

The comparative efficacy of Phyllanthus emblica fruit extract, and its main constituent, ascorbic acid, in modifying the cytotoxic action of lead and aluminium was evaluated in vivo in bone marrow cells of Mus musculus. Oral administration of Phyllanthus emblica fruit extract for 7 days before exposure to the metals through intraperitoneal injections reduced the frequency of micronuclei induced by all doses of both metals. Priming with comparable doses of synthetic ascorbic acid reduced micronuclei formation induced by both doses of aluminium and only the lower dose of lead. With the higher dose of lead (20 mg/kg body wt.) priming with ascorbic acid increased the frequency of micronuclei when compared with mice administered lead alone. The greater efficacy of Phyllanthus fruit extract in alleviating metal-induced clastogenicity may be due to the combined action of all ingredients in the crude extract, rather than to ascorbic acid alone.

Modifying role of Phyllanthus emblica and ascorbic acid against nickel clastogenicity in mice.

Nickel, a major environmental pollutant is known for its clastogenic and carcinogenic potential. Dietary inhibitors of mutagenesis and carcinogenesis are of particular importance since they may have a role in cancer prevention. In the present investigation, aqueous extract of edible dried fruits of Phyllanthus emblica, a well known medicinal plant, was fed to Mus musculus for seven consecutive days prior to treatment with different doses of nickel chloride (10, 20 and 40 mg/kg body wt.); the fruit extract significantly reduced the frequency of CA/cell, the percentage of aberrant cells and the frequency of micronuclei induced by all doses of nickel in the bone marrow cells of mice. Ascorbic acid, a major constituent of the fruit, fed for 7 consecutive days in equivalent concentration as that present in the fruit, however, could only alleviate the cytotoxic effects induced by low doses of nickel; at the higher doses it was ineffective. The greater efficacy of the fruit extract could be due to the interaction of its various natural components rather than to any single constituent. The study assumes importance in view of the widespread human exposure to nickel compounds.

Modification of clastogenicity of lead and aluminium in mouse bone marrow cells by dietary ingestion of Phyllanthus emblica fruit extract.

Extract of Phyllanthus emblica fruit and ascorbic acid were evaluated separately for protection against clastogenicity induced by lead (Pb) and aluminium (Al) salts on mouse bone marrow chromosomes. Oral administration of Phyllanthus fruit extract (PFE) for 7 days before exposure to both metals by intraperitoneal injection increased the frequency of cell division and reduced the frequency of chromosome breaks significantly. Comparable doses of synthetic ascorbic acid (AA) were less effective and could protect against the effects of Al and only a low dose of Pb (10 mg/kg body weight). AA administered before treatment in mice given higher doses of Pb (40 mg/kg body weight) enhanced the frequency of chromosome breaks, giving a synergistic effect. The higher protection afforded by PFE may be due to the combined action of all ingredients, rather than to AA alone.