Disease relevance of PHOSPHAMIDON

• The administered doses were low, as compared with those of the experiments in vitro: the minimal doses inducing chromosome aberrations in vivo were, in the aldrin treatments 9.56, and in the phosphamidon treatments, 0.07 mug/g body weight [1].
• Cytochrome-c oxidase and Mg2+ ATPase activity levels were also decreased considerably, suggesting impaired energy synthesis and breakdown during phosphamidon toxicity, as a result of reduced oxidation of glucose aerobically [2].
• The genotoxic effect of phosphamidon in mice in an in vivo test system was investigated by 3 different assays: chromosomal aberration, micronucleus and sperm-shape abnormality [3].
• Disseminated visceral coccidiosis (DVC) was unexpectedly recognized in a wild white-naped crane (Grus vipio) killed by phosphamidon insecticide [4].
• Ventricular arrhythmias as premature ventricular beats, or bigeminies, were noted with increasing frequency following perfusion with increasing doses of phosphamidon [5].

Psychiatry related information on PHOSPHAMIDON

• Daily decrease was observed in ambulation, rearing and preening responses, with maximum decrement on the seventh day of Dimecron intoxication [6].

High impact information on PHOSPHAMIDON

• Both PHO and DED proved able to induce a dose-dependent increase of micronucleated polychromatic erythrocytes (PCE) [7].
• Two pesticides, organophosphate phosphamidon (PHO) and organochlorine dieldrin (DED) were assayed by the mouse bone marrow micronucleus test, to ascertain whether they showed genotoxic activity in vivo [7].
• Vitamin C, when administered concurrently with a pesticide (endosulfan, phosphamidon or mancozeb), could significantly decrease the frequency of pesticide-induced clastogenic and mitosis-disruptive changes in the bone marrow cells of young Swiss albino mice [8].
• Phosphamidon caused a positive inotropic effect, as indicated by increased maximum time derivative of left ventricular pressure and increased cardiac output [9].
• Phosphamidon had in this preparation a biphasic effect on heart rate: at 10(-6) M concentration, heart rate increased, but at higher concentrations (10(-4)-10(-3) M) heart rate decreased significantly [9].

Chemical compound and disease context of PHOSPHAMIDON

• The acute toxicity of fonofos and phosphamidon on three age classes of Artemia salina was evaluated [10].
• Toxicity of these insecticides are in the order: fenvalerate greater than DDT greater than carbaryl greater than phosphamidon [11].

Biological context of PHOSPHAMIDON

• Since, in the phosphamidon treatments, the cellular death begins at a concentration above 244 mug/ml, the chromosome aberrations, induced especially by the low doses, could be maintained in other abnormal cells [1].
• The comparative cytogenetic effects of aldrin and phosphamidon [1].
• Impact of phosphamidon on the carbohydrate metabolism of a freshwater prawn, Macrobrachium lamarrei [12].
• Studies on the effect of dimecron on the digestive system of a fresh water fish, Channa punctatus [13].
• This possibly indicates that phosphamidon is more embryotoxic during the post-implantation period (day 7) and during late organogenesis (day 13) as compared to the early organogenesis period (day 10) [14].

Anatomical context of PHOSPHAMIDON

• Dimecron is mutagenic to the somatic and germ line cells of Drosophila and induces a high frequency of sex-linked recessive lethals [15].
• The ameliorating effect of vitamin C (injected intraperitoneally) was evaluated against changes in sperm count and sperm head morphology in mice fed either 3, 6 or 1000 mg/kg body wt/day endosulfan, phosphamidon or mancozeb, respectively [16].
• Effects of dimecron on developing chick embryo: malformations and other histopathological changes [17].
• When Wistar strain male albino rats were fed on drinking water containing phosphamidon at 35 ppm concentration for 30 days, the spermatogenic compartment of the testis underwent histopathological changes [18].
• Neurochemical effects of phosphamidon on lipid fractions & lipid peroxidation in the rat central nervous system [19].

Associations of PHOSPHAMIDON with other chemical compounds

• The distribution of insecticides in human body tissues in five cases of poisoning by ethyl parathion, malathion, dimethoate, sumithion and phosphamidon has also been studied [20].
• In vivo recovery of acetylcholinesterase activity from phosphamidon and methylparathion induced inhibition in the nervous tissue of penaeid prawn (Metapenaeus monoceros) [21].
• Sensitivity of selected zooplankton exposed to phosphamidon, fenitrothion, and fenthion [22].
• Cardiac cycle length did not change significantly following perfusion with phosphamidon or obidoxime alone; however, following perfusion with PD/OB, RR significantly increased at high concentrations (10(-3) M) of both drugs [5].
• The inhibition of MAO-A by MCP is reversible whereas the inhibition by DDVP and phosphamidon is irreversible [23].

Gene context of PHOSPHAMIDON

• Data indicate that catalase causes a decrease only in the damage induced by phosphamidon, while glutathione peroxidase protects against damage induced by both phosphamidon and dieldrin [24].
• An organochlorinated pesticide (aldrin) and an organophosphorus one (phosphamidon) were administered in human lymphocyte cultures, and the cytogenetic effects were related to the compound concentration [1].
• Nuvan-exposed third-instar larvae exhibited a 1.2-fold to 1.5-fold greater hsp70 expression compared to Dimecron at concentrations ranging from 0.0075 to 0.075 ppm following 12 and 18 h exposure [25].
• Interaction of phosphamidon with neuropathy target esterase and acetylcholinesterase of hen brain [26].
• Histochemical tests revealed that alkaline phosphatase and glucose-6-phosphatase were inhibited by Dimecron treatment [13].

Analytical, diagnostic and therapeutic context of PHOSPHAMIDON

• Stroke work and total pressure-volume area increased in a dose-dependent manner following perfusion with phosphamidon [9].
• Phosphamidon, one of the organophosphorus compounds studied, showed complete degradation of the DNA after treatment [27].
• Oral administration of phosphamidon in doses of 0.25 and 0.5 mg/kg per day for 120 days caused significant inactivation of carboxylesterase activity (16-32%) without eliciting any intoxicating signs apart from mild intermittent diarrhoea in the animals receiving the higher dose [28].
• Phosphamidon was detected by thin-layer chromatography (TLC) from various CNS regions of the rats intoxicated with three doses (1.0, 1.5 and 2.0 mg/kg body-weight) intraperitoneally daily for seven days [29].

References