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1.
Niger J Physiol Sci ; 28(2): 205-10, 2013 Dec 20.
Article in English | MEDLINE | ID: mdl-24937398

ABSTRACT

Drugs and life style choices such as alcohol consumption and smoking are capable of independently altering levels of essential trace elements as well as tissue or organ function. The purpose of the study is to determine how differences in degree of exposure to cigarette smoke and alcohol consumption will alter serum magnesium (Mg), Cobalt (Co) and Manganese (Mn) levels in female subjects using combined oral contraceptives. Thirty female subjects who have used combined oral contraceptive for at least 5 years as well as 30 age-matched control women who are using rhythm method as birth control method were recruited from drinking joints/bars by random sampling technique. Serum trace element concentrations were determined using atomic absorption spectrometry and K+, Na+, albumin, globulin, total protein, urea and creatinine were also determined. Data obtained were analyzed using Student't' test, Pearson's correlation coefficient and Multivariate Analysis of Variance (MANOVA). Na+ was significantly higher in combined oral contraceptive users compared with controls (p<0.05), whereas Mg was decreased (p<0.05). Co, Mn, urea, creatinine, total protein, albumin, globulin, K+ were not significantly different in combined oral contraceptive users compared with the controls (p>0.05). MANOVA results revealed that binge drinkers/smokers group recorded a significant lower (p<0.05) magnesium level than the passive smokers/social drinkers group and controls. The results of this study suggest that subjects using combined oral contraceptive, consuming alcohol and exposed to cigarette smoke may be at greater risks of diseases linked with magnesium depletion.


Subject(s)
Alcohol Drinking/adverse effects , Contraceptives, Oral, Combined/adverse effects , Contraceptives, Oral, Hormonal/adverse effects , Kidney/drug effects , Magnesium/blood , Smoking/adverse effects , Adult , Alcohol Drinking/blood , Biomarkers/blood , Cobalt/blood , Female , Humans , Kidney/physiopathology , Life Style , Magnesium Deficiency/blood , Magnesium Deficiency/etiology , Manganese/blood , Multivariate Analysis , Risk Assessment , Risk Factors , Smoking/blood , Young Adult
2.
Niger J Physiol Sci ; 26(2): 151-60, 2011 Dec 20.
Article in English | MEDLINE | ID: mdl-22547184

ABSTRACT

This study was carried out to compare the hepatoprotective effect of methionine on paracetamol treated rats at both the peaks of toxicity and absorption. Female Wistar rats were divided into 17 groups consisting of eight rats per group and treated with different doses of paracetamol/methionine (5:1). Each control rat received 5 ml of physiologic saline. The study was terminated at two different end points -the 4th and 16th hours. Results show that rats administered with toxic doses (1000 mg/kg, 3000 mg/kg, 5000 mg/kg BW) of paracetamol exhibited significant increases in the levels of ALT, AST, γ- GT compared with controls. These increases were much higher at the 16th than 4th hour but serum total protein, albumin and globulin were significantly decreased by the end of the 16th hour. Histology results of rats in the 3000 and 5000 mg/kg (by the end of the 16th hour) confirmed hepatic damage, light microscopic evaluation of liver showed remarkable centrilobular necrosis. Moreover, the presence of mononuclear cells in liver section of rats intoxicated with APAP (5000 mg/kg) suggests a possible involvement of inflammatory process which resulted in regurgitation of bilirubin leading to its elevated level as well as increase activity of ALP. The hepatoprotective effect of methionine, on the other hand, was demonstrated in these rats at the 4th and 16th hours, and both results were comparable and therefore not significantly different but elevation in GGT level still persisted. In conclusion, data obtained from this study suggest that these agents may be capable of inducing GGT, although further study is required to establish a possible relationship between methionine and this enzyme in some other animal species.


Subject(s)
Acetaminophen/antagonists & inhibitors , Acetaminophen/toxicity , Analgesics, Non-Narcotic/antagonists & inhibitors , Analgesics, Non-Narcotic/toxicity , Chemical and Drug Induced Liver Injury/prevention & control , Methionine/pharmacology , Animals , Chemical and Drug Induced Liver Injury/pathology , Female , Liver/enzymology , Liver/pathology , Liver Function Tests , Necrosis , Rats , Rats, Wistar
3.
Niger J Physiol Sci ; 25(2): 129-34, 2010 Nov 28.
Article in English | MEDLINE | ID: mdl-22314951

ABSTRACT

Methionine is an effective antidote in the treatment of paracetamol-induced toxicity but at large doses it has been reported to induce or aggravate a number of pathological conditions. It also alters plasma levels of many vital elements and molecules. This study was designed to identify if the alteration observed for antioxidant vitamins and minerals especially at sub-toxic and toxic levels of exposure in our earlier study of 24-hour exposure period may warrant trace elements supplementation. This was investigated by carrying out a 48-hour study to test the ability of a living organism to restore homeostasis of these vital molecules and elements. The levels of antioxidant minerals and vitamins were estimated in the serum samples obtained from adult male Wistar rats exposed to paracetamol tablets. At 100 mg\kg BW (body weight) vitamin A, niacin, riboflavin, selenium and manganese were not significantly different from the control group. Moreover at 350 mg\kg, all these indices except zinc were not significantly different in the exposed group compared with controls whereas at 1000 mg\kg level of exposure manganese, selenium and vitamin E were not significantly decreased at the end of 48 hours of exposure but copper, niacin and vitamin A were significantly increased in the exposed group compared with the controls. These results suggest that with time the body may be capable of bringing about restoration of the levels of some of these elements\vitamins. This was more evident at 350 mg\kg level of exposure than a higher dose of 1000 mg\kg level.


Subject(s)
Trace Elements , Vitamins , Acetaminophen , Animals , Antioxidants , Male , Methionine , Rats , Rats, Wistar
4.
Niger J Physiol Sci ; 23(1-2): 41-9, 2008.
Article in English | MEDLINE | ID: mdl-19434213

ABSTRACT

Tobacco smoke may be one of the most common sources of cadmium (Cd) in the general population, particularly in the rising population of smokers in developing countries. Although a relationship between both cigarette smoking and environmental Cd contamination with prostate cancer exist, the mechanisms are unclear. Most prospective cohort studies found a positive association between current smoking and a fatal cancer of the prostate. We investigated the interaction between zinc and cadmium and the potential risk of prostate cancer in smokers. Serum cadmium level was significantly (P < 0.001) higher in smokers compared with non-smokers, the level in smokers was three-fold that in non-smokers. In contrast zinc was significantly (P < 0.001) reduced in smokers compared with non-smokers. Unlike Zn, Cu was significantly (P < 0.05) higher in smokers than in non-smokers. Iron (Fe) though higher in smokers was not significantly different. Zinc: cadmium ratio was very significantly (P < 0.001) reduced, implying high cadmium: zinc ratio. This ratio was 4.5-fold the level in non-smokers. Total protein, albumin and total globulin levels were all significantly (P < 0.001) reduced in smokers compared with non-smokers respectively. Potassium (K+) was significantly (P < 0.05) higher in smokers than in non-smokers. Magnesium (Mg) was significantly (p < 0.01) reduced in smokers compared to non-smokers. Altered Zn status culminating in high Cd:Zn ratio appears the central factor in smokers; leading to oxidative stress, DNA damage, mutation, impaired DNA repair, P53 expression, angiogenic effect of Cu and impaired vitamin A metabolism. These converge in the risk of the carcinogenic process, suggesting high Cd: Zn ratio as the critical determinant of the risk of prostate cancer in smokers and possibly a biomarker of susceptibility to this environmental disease.


Subject(s)
Cadmium/blood , Prostatic Neoplasms/etiology , Smoking/blood , Zinc/blood , Adolescent , Adult , Biomarkers/blood , Case-Control Studies , Disease Susceptibility , Humans , Male , Middle Aged , Prostatic Neoplasms/blood , Risk Assessment , Risk Factors , Smoking/adverse effects , Time Factors , Up-Regulation , Young Adult
5.
Biol Trace Elem Res ; 116(1): 43-51, 2007 Apr.
Article in English | MEDLINE | ID: mdl-17634626

ABSTRACT

The relationship between blood lead (Pb) and serum levels of calcium and of neural nutrients such as thiamine and magnesium (Mg) has been determined in a Nigerian population that is occupationally exposed to Pb. Forty-seven male Pb workers were recruited as test subjects and 25 males unexposed to Pb served as controls. The test subjects were classified into three groups, based on severity of exposure to Pb. Blood lead (BPb) and the serum levels of Mg, thiamine, and calcium were determined in both test subjects and controls. The mean blood Pb level was not significantly higher in Pb workers. In contrast, Mg and thiamine levels were significantly decreased (p<0.05; p<0.01, respectively). However, the calcium level was not significantly lower in test subjects than in controls. Also, there was a significant negative correlation between serum thiamine and blood Pb levels (r=-0.50; p<0.01). Furthermore, there was a significant negative correlation between serum calcium and BPb levels (r=-0.41; p<0.01). This study has shown that relatively low BPb levels can enhance Pb absorption and also potentiate Pb neurotoxicity in the presence of decreased serum thiamine and Mg levels.


Subject(s)
Lead/blood , Lead/toxicity , Magnesium/blood , Nervous System/drug effects , Occupational Exposure , Thiamine/blood , Adult , Calcium/blood , Humans , Lead Poisoning/blood , Lead Poisoning/diagnosis , Magnesium/therapeutic use , Male , Middle Aged , Models, Chemical , Neurotoxicity Syndromes/etiology , Neurotoxins/pharmacology , Occupational Diseases/etiology
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