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PubMed1975

Bromism: recent perspectives.

The introduction of bromureides on a large scale in England and Australia has resulted in a major health hazard. Attention is directed to this problem so preventive measures may be taken in this country to discourage their marketing. We recommend that physicians acquaint themselves with the active ingredients of over-the-counter sedatives and cough medications and that they consider the potential risks involved before prescribing bromides in organic combination. We maintain that bromism is not a relic of the past but rather a serious problem in some countries and a potential one in ours. In addition to reviewing the present status of bromide intoxication in the United States and abroad, we report an atypical case of possible bromide intoxication from a water supply in a rural area of the Midwest United States. Because of reports of bromide intoxication in rural areas, we speculate that some of these cases may be secondary to contaminated water supplies.

Adult↗
PubMed2000

Study of the neurochemical alterations produced in discrete brain areas by perinatal low-level lead exposure.

Although the neurotoxic effects of Pb are well documented, the subcellular mechanisms of this action in the central nervous system are not fully understood. The present work examines some neurochemical parameters in discrete brain areas of pups whose mothers were intoxicated via drinking water with lead (300 mg/L), from day 1 of pregnancy until postnatal day 12. Lead intoxication produced a significant reduction in the activity of the enzymes alkaline phosphatase and ATP-ase in the brain. Furthermore, the levels of adenine nucleotides were significantly altered by treatment, the striatum being the area more affected, whereas lead did not vary the levels of ATP, ADP and AMP in the hypothalamus. On the other hand, there was a general decrease in neurotransmitter levels in all areas, specially in the hippocampus. These data suggest that gestational and lactational exposure to low dose of lead could produce neurochemical changes in discrete brain areas which can be responsible for the neurophysiological and behavioral changes described in lead-intoxicated animals.

Adenosine Triphosphatases↗
PubMed2006

[Effect of 1, 2-dichloroethane on blood brain barrier].

OBJECTIVE: To investigate the effect of 1, 2-dichloroethane (1, 2-DCE) on blood brain barrier. METHODS: Acute toxic encephalopathy model was copied with the consecutive static inhalation of 1, 2-DCE. The water content of brain tissue was measured, and the blood brain barrier permeability was detected with lanthanum nitrate. The brain microvascular endothelial cells and neuroglial cells were cultured in vitro, which were administrated with 1, 2-DCE. The cell morphologic structures were observed under light microscope and electron microscope. RESULTS: (1) The extracellular edema was most found in the cerebral tissue and the leakage of lanthanum particles through the barrier were found with the lanthanum tracking method. (2) The water content in cerebral cortex in the moderate and high dose groups was significantly higher than that in the control group and became severer with the increases of the intoxicated time. The water content in cerebral medulla was significantly increased only at 6 hours after the intoxication. (3) The normal morphological structure of brain microvascular endothelial cells and neuroglial cells could be injured by 1, 2-DCE, and the injury to neuroglial cells caused by 1, 2-DCE occurred earlier and severer than that to brain microvascular endothelial cells. CONCLUSION: 1, 2-DCE can damage blood brain barrier and induce cerebral edema.

Administration, Inhalation↗
PubMed2001

Differential effects of lead and zinc on inhibitory avoidance learning in mice.

We studied the effects of chronic intoxication with the heavy metals lead (Pb2+) and zinc (Zn2+) on memory formation in mice. Animals were intoxicated through drinking water during the pre- and postnatal periods and then tested in the step-through inhibitory avoidance memory task. Chronic postnatal intoxication with Pb2+ did not change the step-through latency values recorded during the 4 weeks of the test (ANOVA, P>0.05). In contrast, mice intoxicated during the prenatal period showed significantly reduced latency values when compared to the control group (day 1: q = 4.62, P<0.05; day 7: q = 4.42, P<0.05; day 14: q = 5.65, P<0.05; day 21: q = 3.96, P<0.05, and day 28: q = 6.09, P<0.05). Although chronic postnatal intoxication with Zn2+ did not alter a memory retention test performed 24 h after training, we noticed a gradual decrease in latency at subsequent 4-week intervals (F = 3.07, P<0.05), an effect that was not observed in the control or in the Pb2+-treated groups. These results suggest an impairment of memory formation by Pb2+ when the animals are exposed during the critical period of neurogenesis, while Zn2+ appears to facilitate learning extinction.

Animals↗
PubMed1995

Chemical and biological demonstration of the presence of monofluoroacetate in the leaves of Palicourea marcgravii St. Hil.

Cattle losses in Brazil have been attributed to Palicourea marcgravii St. Hil., a toxic plant for cattle. The crude extract from the leaves of P. marcgravii was successively fractionated using solvents with different polarities to determine whether monofluoroacetic acid and/or some other substance present in the leaves may be responsible for the acute symptoms caused by the plant. Authentic sodium monofluoroacetate (SMFA) was used for comparison. The only P. marcgravii fraction which induced seizures and death in intoxicated rats was water soluble. The signs and symptoms induced in the animals by the crude extract and water-soluble fraction were the same as induced by SMFA and included tonic seizures and other actions on the CNS. The dose-lethality and dose-latency to the 1st seizure curves constructed for the water-soluble fraction of the leaf extract (30-100 mg/kg) and SMFA (0.6-3.0 mg/kg) were parallel. Five animals per dose were used. The potency ratio of SMFA in relation to the water-soluble fraction of the leaf extract was 53.8 (dose-lethality curve) and 64.1 (dose-latency to the 1st seizure curve). The water-soluble fraction contained a substance with hRf = 20 which was the same as that of authentic SMFA. The 19F NMR spectra of authentic SMFA and the P. marcgravii water-soluble fraction were identical. These data demonstrate the presence of SMFA in the water-soluble fraction of P. marcgravii leaves and show that monofluoroacetate is the active principle responsible for the signs and symptoms of acute intoxication.

Animals↗
PubMed1978

Lithium intoxication. (Report of 23 cases and review of 100 cases from the literature).

Twenty-three patients were studied, 21 of whom developed intoxication during maintenance therapy with a lithium dosage which had been unchanged for months to years. Toxic effects on brain, heart and kidneys were found and the severity of lithium intoxication seemed to depend on at least three factors: the height of the serum lithium concentration (SLi), the duration of lithium intoxication and individual tolerance. Disorders of water and electrolyte metabolism preceded lithium intoxication in the majority of the patients. Water loss due to impaired renal concentrating ability seemed to be a major predisposing factor. Renal insufficiency was apparent in 17 of the patients on admission and five of these did not regain normal renal function. In seven patients, renal biopsy showed abnormalities which suggest that a chronic nephropathy, possibly caused by lithium, might be another predisposing factor. Treatment with sodium chloride infusion had no specific effect on lithium excretion and led to hypernatraemia in some patients and is therefore not recommended. Hemodialysis is the most effective method available for removing the lithium ion from intoxicated patients. Hemodialysis should be carried out long enough to secure a SLi of less than 1 mmol/l after redistribution of lithium in the body. Treatment by peritoneal dialysis is appropriate only if hemodialysis facilities are unavailable. Lithium intoxication is a serious condition. Of the 23 patients reported, two died and two developed persisting neurological sequelae. The best way to prevent lithium intoxication is to control the serum concentration and to assess renal function and renal concentrating ability regularly during therapy.

Acute Kidney Injury↗
PubMed1999

Age-dependent acrylamide neurotoxicity in mice: morphology, physiology, and function.

Acrylamide intoxication produces peripheral neuropathy characterized by weakness and ataxia in both humans and experimental animals. Previous studies on animals of different ages and species indicate that the longest and largest nerves are affected earlier with the major pathology in the terminal parts of axons, i.e., distal axonopathy. However, several issues have remained elusive; for example, what are the earliest pathological changes? An equally intriguing question is whether younger animals are more susceptible to acrylamide than older animals. To address these issues, we compared the vulnerability to acrylamide of 3- and 8-week-old mice. These mice were intoxicated with acrylamide in drinking water (400 ppm). The sequence of intoxication could be categorized into three stages. In the initial stage, there was no visible weakness or ataxia. The only noticeable changes were poor performance on the rota-rod test and swelling of motor nerve terminals. Obvious weakness and ataxia of hindlimbs developed gradually (here designated as the early stage). The weakness and ataxia progressed at variable speeds in mice of different ages, and eventually the forelimbs (quadriparesis) were affected in the late stage. Each stage appeared earlier in 3-week-old mice than in 8-week-old mice (7.1 +/- 1.1 vs 15.6 +/- 4.0 days, P < 0.01 for the early stage; and 15.3 +/- 2.1 vs 31.7 +/- 6.0 days, P < 0.01 for the late stage). The progression of neurological deficits was also faster in the younger mice (7.2 +/- 1.8 vs 16.3 +/- 4.2 days, P < 0.01). Pathological changes in the distal parts of motor nerves innervating hindfoot muscles were evaluated by combined cholinesterase histochemistry and immunocytochemistry for neuronal markers to demonstrate motor nerve terminals and neuromuscular junctions simultaneously. In the initial stage, there was axonal swelling in motor nerve terminals. As acrylamide intoxication continued, axonal swelling extended into junctional folds and into the intramuscular nerves, which resulted in Wallerian-like degeneration. Our results indicate that younger mice show a much higher susceptibility to acrylamide intoxication, and pathological changes precede neurological symptoms.

Acrylamide↗
PubMed1978

[Dermatologic aspects of arsenic poisoning caused by drinking water].

The dermal aspects of an accumulated familiar arsenical late-intoxication -- caused by drinking-water -- are described. We have to expect similar cases to this one even today. At the appearance of multiple M. Bowencentres we have to consider in addition to inner-organic carcinoma, the possibility of an arsenical intoxication as well.

Adult↗
PubMed2003

Recommendations for return to sports following cervical spine injuries.

The decision of return to play following cervical spine injuries can be one of the most challenging with a wide variation in opinion as far as management. The onus is on the physician to consider the risks of continued play for patients who have experienced a cervical spine injury and who are reluctant to give up their sport of choice. In general, the literature shows agreement for the basic necessities for return to collision sports to include: normal strength, painless range of motion, a stable vertebral column and adequate space for the neurological elements. In addition, return to play in an unsafe environment is contraindicated. Playing with defective equipment or with improper technique has been associated with catastrophic injuries and should be avoided. This particularly includes: spear tackling, diving in unknown or shallow water, diving while intoxicated, checking from behind in hockey or using a trampoline without spotting equipment. However, there is a lack of consensus on returning to play with the following: stenosis, spear tackler's spine, loss of normal lordosis or range of motion, surgically corrected instability, ligamentous instability less than that defined by White/Panjabi, transient quadriparesis, healed disc herniation and congenital fusion. More informed decisions can be made by physician and patient using a basic knowledge of: (i) previous clinical experience, including that outlined in published epidemiological studies and guidelines; (ii) biomechanical data defined in the laboratory; and (iii) the priorities of the patient.

Athletic Injuries↗
PubMed2005

Toxicokinetics of mercury elimination by succimer in twin toddlers.

We describe the toxicokinetics of mercury in two twin toddlers poisoned by an East Indian remedy for teething. Succimer (dimercaprosuccinic acid, DMSA) decreased the plasma elimination half-life of mercury by 3-fold in the patient with high exposure; a more modest effect was observed in the other twin. Succimer is a chelation agent used in the treatment of heavy metal intoxication. A water-soluble agent, it increases the urinary excretion of lead and mercury. The drug is rapidly but variably absorbed through the gastrointestinal tract, with peak levels occurring at 1-2 hours. After its absorption, peak mercury excretion through the urine occurs within 2-4 hours. In the poisoned twin sisters, succimer administration led to a mercury plasma elimination half-life of 6 weeks. Although succimer has been used in mercury poisoning in adults and children, the toxicokinetics of mercury have not previously been characterized in either age group. We believe this is the first such description. More studies on the toxicokinetics and dynamics of mercury chelation with succimer in young children are needed to ensure the optimal use of the drug in this population.

Antidotes↗
PubMed1992

Idiopathic immune-mediated hemolytic anemia in a calf.

Severe anemia was found in a 4-month-old heifer, which was admitted with a 1-day history of anorexia, signs of depression, and recumbency. A diagnosis of immune-mediated hemolytic anemia (IHA) was made on the basis of a Coomb's titer of 1:128 and decreased resistance to osmotic stress, as determined by an RBC fragility test. Anaplasmosis and leptospirosis were ruled out as possible causes of the IHA. Other causes of hemolytic anemia, including intoxication by copper, water, Brassica spp, or drugs were ruled out. Therefore the IHA was considered idiopathic. Treatment consisted of supportive therapy, oxytetracycline, and dexamethasone. After 60 days of treatment, CBC, Coomb's test result, and RBC fragility were within normal limits.

Anemia, Hemolytic, Autoimmune↗
PubMed1980

[Endemic Balkan nephropathy (author's transl)].

Endemic Balkan nephropathy (EBN) is a chronic interstitial nephritis which may occur at any age and may affect several members of the same family. The condition is slowly progressive and can more easily be diagnosed in its advanced than in its early stages. Early symptoms include severe anaemia and increased plasma aminoacids, alkaline phosphatases and gamma 2 and alpha globulins. Eosinophilia is not uncommon. Loss of urine concentration power and high beta 2 microglobin urinary levels are among the earliest signs of EBN and of considerable diagnostic value. Renal biopsy shows invasive sclerosis, IgG and IgA deposits in glomerular vessels and Bowman's capsule walls and, characteristically, osmiophilic granulations within the mitochondria of proximal tubule cells; the mitochondria may in due course burst and disappear. Atrophic or dystrophic changes may develop in the stomach, upper intestine and liver. The aetiology of EBN remains undetermined, but chronic intoxication with drinking water polluted by silicates released during soil erosion seems to be the most probable cause. Silicates may act directly or by inducing an immune process.

Adolescent↗
PubMed1998

[Lead intoxication and amyotrophic lateral sclerosis].

A seventy-six-year-old patient developed a bulbar form of amyotrophic lateral sclerosis, after chronic lead intoxication from drinking water. Treatment with 2,3 dimercaptosuccinic acid was administered for six months and had no effect on clinical course. We discuss the imputability of lead as a possible etiological factor.

Aged↗