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T Hussain

Publications and source records attributed to T Hussain.

At least 37 records · Page 2Linked to original sources
PubMed2001

Role of endothelium in adenosine receptor-mediated vasorelaxation in hypertensive rats.

The present study was designed to investigate the role of endothelium derived relaxing factor nitric oxide (NO) in adenosine A2 receptor mediated vasorelaxation in normotensive (WKY) and hypertensive (SHR) rat aortic ring preparations. Adenosine analogues, 2-chloroadenosine (CAD) and 5-ethylcarboxamidoadenosine (NECA) produced concentration-dependent (10(-9)-10(-4) M) relaxation in phenylephrine (1 x 10(-6) M) precontracted vascular rings, which was significantly shifted to the right in SHR compared to WKY rats. Endothelium removal attenuated CAD and NECA relaxation responses in both SHR and WKY and abolished the difference in relaxation between SHR and WKY vascular tissues. The relaxation response to CAD was antagonised by adenosine A2 receptor antagonist, 8-sulfophenyltheophylline (8-SPT, 50 x 10(-6) M). The antagonism by 8-SPT was lower in SHR as compared to WKY tissues. L-monomethylarginine (L-LMMA) (30 x 10(-6) M) significantly shifted the CAD relaxation to the right, which was reversed by the addition of L-arginine (100 x 10(-6) M) in both SHR and WKY rats. However, the rightward shift by L-NMMA was smaller in SHR compared to WKY vascular tissues. Vasorelaxation response to acetylcholine (1 x 10(-6) M) was significantly inhibited (50%) in SHR rings compared to WKY. The relaxation produced by sodium nitroprusside (10(-9)-10(-5) M) in endothelium-intact and -denuded aortic rings showed no difference between SHR and WKY. Isoproterenol produced concentration-dependent (10-9-10-5 M) relaxation, which was shifted to the right in SHR compared to WKY rings with an intact endothelium, while the removal of endothelium abolished the difference in the response between SHR and WKY. The results suggest: (i) adenosine A2 receptors mediate vasorelaxation in part through endothelium possibly by releasing nitric oxide (NO); (ii) the impairment of endothelium may be one of the factors for the attenuation of adenosine receptor and receptor-mediated responses in SHR.

Adenosine↗
PubMed2001

Dopamine fails to inhibit Na,H-exchanger in proximal tubules of obese Zucker rats.

Dopamine via the activation of D1-like receptors inhibits Na,K-ATPase and Na,H-exchanger and subsequently increases sodium excretion. We have previously reported that dopamine failed to inhibit Na,K-ATPase in the proximal tubules (PTs) of obese Zucker rats. The present study was designed to determine the effect of dopamine on Na,H-exchanger in PTs of lean and obese Zucker rats, and examine D1-like receptor-coupled signal transduction pathway mediating the inhibition of Na,H-exchanger. We found that dopamine inhibited Na,H-exchanger in the PTs of lean rats but this response was absent in obese rats. In brush border membranes, [3H]SCH 23390 binding revealed a approximately 45% reduction in D1-like receptor binding sites in obese compared to lean rats. Dopamine stimulated cAMP accumulation in PTs of lean but not in obese rats. Forskolin-mediated stimulation of cAMP was similar in lean and obese rats. Dopamine as well as forskolin and dibutyryl cAMP-mediated stimulation of protein kinase A (PKA) was reduced in PTs of obese compared to lean rats. The data suggest that reduction in D1-like receptor binding sites, defective coupling with signaling pathway and inability of PKA activation may be responsible for the failure of dopamine to inhibit Na,H-exchanger in PTs of obese rats. This phenomenon may contribute to an increase in sodium reabsorption and development of hypertension in obese Zucker rats.

Animals↗
PubMed2000

Defective renal dopamine D1-like receptor signal transduction in obese hypertensive rats.

It is reported that dopamine promotes renal sodium excretion via activation of D1-like dopamine receptors located on the proximal tubules. In spontaneously hypertensive rats the natriuretic and diuretic response to exogenously administered and endogenously produced dopamine is reduced, which results from a diminished dopamine-induced inhibition of the enzyme, Na+,K+-ATPase. The present study was designed to examine dopamine-receptor mediated inhibition of Na+,K+-ATPase and its associated signal transduction pathway in the proximal tubules of Zucker obese and lean control rats. The obese animals were hypertensive, hyperinsulinaemic and hyperglycaemic compared with the lean rats. While dopamine caused inhibition of Na+,K+-ATPase activity in lean rats, this effect was significantly attenuated in the obese animals. There was significant reduction in D1-like receptor numbers in the basolateral membranes of obese rats compared with lean rats with no change in the affinity to the ligand [3H]SCH 23390 between the two groups of rats. Dopamine failed to stimulate G proteins as measured by [35S]GTPgammaS binding in the obese rats. Also, dopamine was unable to cause phospholipase-C activation in obese rats, but it did activate phospholipase-C in lean rats. These results show that reduction in D1-like receptor numbers and a defect in receptor-G protein coupling may account for the inability of dopamine to activate the D1-like receptor-coupled signal transduction pathway and cause inhibition of Na+,K+-ATPase in the obese hypertensive rats.

Animals↗
PubMed2000

Diminished natriuretic response to dopamine in old rats is due to an impaired D1-like receptor-signaling pathway.

BACKGROUND: Dopamine (DA) causes natriuresis and diuresis, which results from activation of D1-like receptor (D1R) located on proximal tubules. Earlier, we reported that DA failed to inhibit Na,K-ATPase in proximal tubules of old Fischer 344 rats. The present study was designed to investigate the functional consequence of this phenomenon. METHODS: Measurements of the functional (natriuretic and diuretic) response to intravenously infused DA and SKF 38393 (D1R agonist) in adult (6 month) and old (24 month) Fischer 344 rats were taken. Biochemical measurements were carried out to determine the potential defects in D1R and its signaling pathway in proximal tubules of old rats. RESULTS: We found that intravenous infusion of DA and SKF 38393 caused natriuresis and diuresis in adult rats, but this response was blunted in old rats. In the isolated proximal tubules, DA and SKF 38393 inhibited Na,H-exchanger (NHE) in adult rats; however, this inhibition was attenuated in old rats. Radioligand binding revealed approximately 46% reduction in D1R binding sites in brush border membranes (BBMs) in old compared with adult rats. SKF 38393 stimulated [35S]GTPgammaS binding in BBM in adult rats, but not in old rats, suggesting an impaired D1R-G protein coupling. DA and SKF 38393 stimulated adenylyl cyclase (AC) activity in adult but not in the old rats. Forskolin and NaF stimulated AC activity in a comparable manner in adult and old rats, indicating no defect in AC and G proteins. DA and SKF 38393 failed to stimulate protein kinase A (PKA) activity in proximal tubules of old rats. Dibutyryl-cAMP-mediated PKA activation was also absent in old rats. CONCLUSIONS: A decrease in D1R binding sites, a coupling defect with G proteins, and a defect in PKA activation lead to diminished DA-mediated inhibition of NHE in old rats, which may contribute to the blunted natriuretic response to DA in these animals.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2000

Dopamine inhibits na,h-exchanger via D1-like receptor-mediated stimulation of protein kinase a in renal proximal tubules.

Dopamine causes natriuresis and diuresis via activation of D1-like receptors located in the renal proximal tubules. It is reported that this response to dopamine results from the inhibition of Na,H-exchanger and Na,K-ATPase. Earlier studies have suggested a role of protein kinase A (PKA) in the inhibition of Na,H-exchanger, however, the effect of dopamine or the dopamine receptor subtype responsible for the stimulation of PKA has not been reported. Present study was designed to examine the effect of dopamine and D1-like receptor agonist, SKF 38393, on the stimulation of PKA activity in rat renal proximal tubules. Dopamine and SKF 38393 (1 nM - 1 microM) caused stimulation of PKA activity, an effect which was antagonized by a D1-like receptor antagonist, SCH 23390 (10 microM). Stimulation of PKA activity was also seen with forskolin and di-butyryl cAMP. We also observed that dopamine and SKF 38393 inhibited Na,H-exchanger activity in the proximal tubules. This response was blocked by SCH 23390 and Rp-cAMPS triethylamine, a selective inhibitor of PKA. Similarly, forskolin and di-butyryl cAMP inhibited Na,H-exchanger activity. The data provide direct evidence showing that dopamine, through the activation of D1-like receptors stimulates PKA activity which in turn inhibits Na,H-exchanger in the proximal tubules.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2000

Respiratory symptoms and wheat flour exposure: a study of flour millers.

The objective of this study was to determine the prevalence of respiratory symptoms and their relationship to sensitization to wheat flour allergens and fungal amylase, in a group of workers from the UK flour milling industry. A cross-sectional study was used to evaluate symptoms, using a structured interview technique, and sensitization, using skin prick test findings, from 679 employees in flour milling and packing operations at 18 flour mills. A total of 147 workers (147/679, 22%) described upper respiratory tract symptoms of some kind. In the majority (139/147, 95%) these symptoms were of an occasional or transitory nature and were related to short-term exposures to high levels of dust. Three individuals (3/679, 0.4%) were identified whose symptoms were thought to be the result of allergy to wheat flour. The prevalence of positive skin prick tests to wheat flour allergens and to fungal amylase was 1.2% (8/678) and 0.9% (6/678), respectively. Measurements of total inhalable dust exposure for personnel exposed to flour dust were taken at 10 of the sites (116 samples). For production personnel the levels were typically between 1 and 10 mg/m3 (8-h time weighted average), with a median of 6.2 mg/m3. Hygiene operatives had appreciably higher exposure than production personnel, with a median of 18.7 mg/m3. Overall, 43% (50/116) of all samples exceeded 10 mg/m3 (8-h time weighted average). The findings suggest that the risk of sensitization to wheat flour allergens from current dust exposures in flour mills is very low. Wheat allergy was responsible in only a small proportion of the total who had respiratory symptoms. The principal causation of symptoms experienced by the workforce was considered to be a non-specific irritant effect related to short-term exposures to high levels of total inhalable dust.

Amylases↗
PubMed2000

PediaSure in the treatment of severe malnutrition in Pakistani children.

OBJECTIVES: We used "PediaSure" a high-density supplemental high caloric feed, for the purpose of nutrition therapy of malnourished children during the initial 2 weeks of rehabilitation. METHODOLOGY: Thirty-one severely malnourished children between the ages of 1-5 years of age completed the study. After management of acute medical complications, they were started on "Pediasure" as their source of calories, for 2 weeks. Their weight gain clinical tolerance, stool output were monitored, as were hematological and biochemical parameters. RESULTS: The study revealed a significant increase in caloric intake (p < 0.01) at the end of 2 weeks. There was also a significant improvement in weight gain of these children, averaging to 7.5 gm/kg/day. The Z score weight for age improved as well, (p = < 0.01) over the 2 week period. The biochemical parameters registered an increase in their serum potassium levels, but no untoward chemical imbalance was noted. Tolerance for PediSure was very high, only one child was excluded from the study due to limited intake. None of the children developed diarrhea. CONCLUSION: We conclude that "PediaSure" can be used effectively in the initial stage of nutrition rehabilitation of severely malnourished children.

Child, Preschool↗
PubMed1999

Vascular surgical society of great britain and ireland: twenty-three years of experience of carotid endarterectomy

BACKGROUND: Carotid endarterectomy (CEA) has been an evidence-based treatment for symptomatic severe carotid stenosis since 1991. Surgical techniques and patient selection have changed over the years. The results of CEA in a single centre over a 23-year period were reviewed. METHODS: Prospectively gathered preoperative, operative, postoperative and long-term follow-up data were analysed. Routine intraoperative shunting and patch closure has been used since 1988. Data were analysed using the chi2 test or by logistic regression, adjusting for age at operation and date of operation. RESULTS: Five hundred and seventy-three CEAs (37 bilateral and three repeat procedures) were carried out on 533 patients. Trainees performed an increasing proportion of CEAs from 1996 to 1998 (15, 50 and 56 per cent respectively). The perioperative death rate was 0.8 per cent and the rate of any perioperative neurological deficit was 6.9 per cent. Other causes of morbidity included nerve injury (5.1 per cent) of which the commonest was to the hypoglossal nerve (2.7 per cent). During follow-up (median 4 (range 0-22) years) there were 81 neurological events (15.9 per cent) which included 35 ipsilateral (6.6 per cent) and 18 contralateral (3.4 per cent) strokes. There was no significant difference in outcome for grade of surgeon, intraoperative shunting or patch closure. Major causes of death were cardiac death (74; 14.6 per cent) followed by stroke (23; 4.5 per cent) and cancer (20; 3.9 per cent). CONCLUSION: The introduction of routine intraoperative shunting and patch closure, as well as allowing surgical trainees to perform supervised CEAs, has not affected perioperative morbidity and mortality rates or long-term outcome.

Journal Article↗
PubMed1999

Changes in serotonin2A and GABA(A) receptors in schizophrenia: studies on the human dorsolateral prefrontal cortex.

Having shown a decrease in serotonin2A receptors in the dorsolateral prefrontal cortex (DLPFC) from schizophrenic subjects, we have now determined if this change was reflective of widespread changes in neurochemical markers in DLPFC in schizophrenia. In Brodmann's area (BA) 9 from 19 schizophrenic and 19 control subjects, we confirmed a decrease in the density of [3H]ketanserin binding to serotonin2A receptors in tissue from the schizophrenic subjects [39 +/- 3.3 vs. 60 +/- 3.6 fmol/mg estimated tissue equivalents (ETE); p < 0.005]. In addition, the density of [3H]muscimol binding to GABA(A) receptors was increased in the schizophrenic subjects (526 +/- 19 vs. 444 +/- 28 fmol/mg ETE; p < 0.02). [3H]YM-09151-2, N-[1-(2-thienyl)cyclohexyl]-3,4-[3H]piperidine, [3H]SCH 23390, [3H]mazindol, and N(G)-nitro-L-[3H]arginine binding to BA 9 did not differ between groups, and there was no specific binding of [3H]raclopride or 7-hydroxy-2-(di-n-[3H]propylamino)tetralin to BA 9 from either cohort of subjects. This suggests the density of dopamine D1-like and NMDA receptors, the dopamine transporter, and nitric oxide synthase activity are not altered in BA 9 from schizophrenic subjects. The selective nature of the changes in serotonin2A and GABA(A) receptors in DLPFC could indicate that these changes are involved in the pathology of schizophrenia.

Adult↗
PubMed1999

Aging, high salt intake, and renal dopaminergic activity in Fischer 344 rats.

The present study examined renal dopaminergic activity and its response to high salt (HS) intake in adult (6-month-old) and old (24-month-old) Fischer 344 rats. Daily urinary excretion of L-3, 4-dihydroxyphenylalanine (L-DOPA), dopamine, and its metabolites 3, 4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid was similar in adult and old rats; by contrast, daily urinary excretion of norepinephrine in old rats was almost twice that in adult animals. HS intake (1% NaCl) over a period of 24 hours resulted in a 2-fold increase in the urinary excretion of dopamine, DOPAC, and norepinephrine in adult animals but not in old animals. Norepinephrine and L-DOPA plasma levels did not change during HS intake and were similar in both groups of rats. The natriuretic response to an HS intake in old rats (from 4.7+/-0.4 to 10.7+/-2.0 nmol. kg(-1). d(-1); Delta=6.0+/-0.9 nmol. kg(-1). d(-1)) was less than in adult rats (from 5.2+/-0.4 to 13.5+/-2.5 nmol. kg(-1). d(-1); Delta=8.3+/-0.8 nmol. kg(-1). d(-1)). A diuretic response to HS intake was observed in adult rats (from 20.9+/-2.3 to 37.6+/-2.8 mL. kg(-1). d(-1)) but not in old rats (from 37.7+/-5.7 to 42.3+/-6. 0 mL. kg(-1). d(-1)). Dopamine levels and dopamine/L-DOPA ratios in the renal cortex of old rats were greater than in adult rats. HS intake increased both dopamine levels and dopamine/L-DOPA ratios in the renal cortex of adult rats but not in old rats. Aromatic L-amino acid decarboxylase activity was higher in old rats than in adult rats; HS intake increased L-amino acid decarboxylase activity (nmol. mg protein(-1). l5 min(-1)) in adult rats (from 67+/-1 to 93+/-1) but not in old rats (from 86+/-2 to 87+/-2). Dopamine inhibited Na(+),K(+)-ATPase activity in proximal tubules obtained from adult rats, but it failed to exert such an inhibitory effect in old rats. It is concluded that renal dopaminergic tonus in old rats is higher than in adult rats but fails to respond to HS intake as observed in adult rats. This may be due in part to the inability of dopamine to inhibit Na(+),K(+)-ATPase activity in old rats.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Defective dopamine receptor function in proximal tubules of obese zucker rats.

Some of the pathophysiological consequences of obesity include insulin resistance, increased renal sodium reabsorption, and the development of hypertension. Dopamine promotes renal sodium excretion via activation of D(1)-like receptors present on the proximal tubules. Reduced dopamine-induced natriuresis and a defect in D(1)-like receptor function have been reported in the proximal tubules of hypertensive animals. The present study investigated D(1)-like dopamine receptors and associated G proteins as the initial signaling components in the proximal tubular basolateral membranes of obese Zucker and control lean Zucker rats. We found that the obese rats were hyperinsulinemic, hyperglycemic, and hypertensive compared with the lean rats. Dopamine produced concentration-dependent inhibition of Na,K-ATPase activity in the proximal tubules of lean rats, whereas the inhibitory effect of dopamine was reduced in obese rats. The D(1)-like receptors measured by [(3)H]SCH 23390 binding revealed an approximately 45% decrease in B(max) without a change in K(d) in the basolateral membranes of obese rats compared with lean rats. Although we found an increase in G(q)/11alpha and no change in G(s)alpha in the basolateral membranes of obese rats, dopamine and SKF 38393 failed to stimulate G proteins as measured by [(35)S]GTPgammaS binding in obese rats, suggesting a receptor-G protein coupling defect. We conclude that decrease in D(1)-like dopamine receptor binding sites and diminished activation of G proteins, resulting perhaps from defective coupling, led to the reduced inhibition by dopamine of Na,K-ATPase activity in the proximal tubules of obese Zucker rats. Such a defect in renal dopamine receptor function may contribute to sodium retention and development of hypertension in obese rats.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1999

Antibodies reacting with chloroquine in human sera.

Presence of antibodies in human sera reacting with chloroquine (CQ) was demonstrated from a malaria endemic belt. The study groups consisted of 53 healthy volunteers, receiving regular chloroquine prophylaxis [2 tablets of CQ (150 mg)/wk, single dose], 105 individuals with a history of frequent CQ intake for any febrile attack and 95 individuals from a non-endemic area who had neither a history of malaria nor of previous consumption of CQ. Sixty six per cent individuals taking regular prophylactic chloroquine and about ten per cent of those with a history of taking frequent chloroquine due to febrile illness in the malaria endemic area showed antibodies reacting to chloroquine. However, antichloroquine antibodies were either insignificant or nondetectable in serum samples collected from persons without any history of chloroquine intake. The results indicate a possible interaction of CQ in vivo.

Antibodies↗
PubMed1999

Presenting features in Pakistani patients suffering from the antineutrophil cytoplasmic antibody--classical subtype (c-ANCA) associated vasculitis.

OBJECTIVES: To study the clinicopathological features in c-ANCA positive patients suffering from vasculitis with a view to find out the most common mode of presentation. STUDY DESIGN: Retrospective. SETTINGS: Department of Immunology, AFIP, Rawalpindi, MH Rawalpindi, CMH Rawalpindi, Department of Rheumatology, PIMS, Islamabad, RGH Rawalpindi, FFH, Rawalpindi. SUBJECTS: Seventeen patients suffering from vasculitis and found to be positive for c-ANCA. MAIN OUTCOME MEASURES: Clinico-pathological features at presentation. RESULTS: There were 9 males in age range 11-60 years (mean age 32.5 years) and 8 females in age range 26-42 years (mean age 32.3 years). Common presenting features were a combination of cough, blocked nose and post nasal drip 14/17 (82%) followed by nose bleed and haematuria 11/17 (65%). Six patients were demonstrated to be suffering from Wegener's granulomatosis after biopsy. C-ANCA was detected by indirect immunofluorescence in the titre range of 8-640. The auto antibody levels related to disease activity. CONCLUSION: c-ANCA associated vasculitis is a rare (17 patients in five years) but aggressive form of vasculitis. It must be suspected in patients with persistent respiratory tract related symptoms associated with fever and joint pains which fail to respond to adequate treatment for infections. The c-ANCA estimations can be utilised as sensitive and specific diagnostic and prognostic marker in this form of vasculitis.

Adolescent↗
PubMed1999

Demographic aspects of hepatitis C in northern Pakistan.

OBJECTIVE: To find out the prevalence of hepatitis C in various, age, sex and ethnic groups in Pakistan. SETTING: Specimens obtained from military/civil hospitals and General Practitioners of Rawalpindi Islamabad, region and other areas of Northern Pakistan, in vicinity. SUBJECTS: Serum of 1710 patients of hepatitis C, diagnosed at Armed Forces Institute of Pathology (AFIP), Rawalpindi between 1st July 1996 and Dec 31, 1997, tested for Anti HCV by 3rd generation Murex Elisa. Required information was collected on a proforma filled for each patient. RESULTS AND CONCLUSION: The majority of the cases were between 30-60 years of age. There was male preponderance. The infection was more common in Urdu speaking fraction of the patients as compared with others.

Adolescent↗
PubMed1998

Cyclic AMP antagonizes adenosine-induced inhibition of ganglionic transmission.

The mechanism of adenosine-induced inhibition of ganglionic transmission was investigated in the isolated superior cervical ganglion (SCG) of the rat. The inhibitory effect of adenosine on the postganglionic compound action potential (CAP) was antagonized by pretreatment of ganglia with forskolin, isoproterenol (IPNE), arginine vasopressin (AVP), or papaverine, all of which are known to increase tissue cAMP level by different mechanisms. Furthermore, pretreatment of ganglia with the adenylate cyclase inhibitor SQ 22, 536, or the phosphodiesterase activator imidazole reversed the effects of IPNE and forskolin. Pretreatment with 8-bromo-cAMP, resulted in a marked antagonism of the adenosine-induced inhibition. By themselves, none of these drugs had any significant effect on the CAP. Adenosine slightly but significantly decreased the basal level of cAMP in untreated ganglia. Formation of cAMP induced by IPNE was markedly reduced by adenosine. This was largely reversed in the presence of the adenosine A1 receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX) but not the A2 receptor antagonist 3, 7-dimethyl-1-propargylxanthine (DPMX). We conclude that the inhibition of ganglionic transmission by adenosine involves reduction of cAMP formation through activation of A1 receptors.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1998

Quantitative ELISA for platelet m-calpain: a phenotypic index for detection of carriers of Duchenne muscular dystrophy.

In order to measure the amount of m-calpain in platelets from Duchenne muscular dystrophy (DMD) patients, carriers and controls, an enzyme linked immunosorbent assay (ELISA) has been developed using polyclonal antibodies raised against m-calpain (Calcium dependent neutral protease), purified from human placenta. Compared to controls a nine-fold increase in the level of m-calpain was observed in all 25 DMD patients and eight obligate carrier mothers studied. Serum creatine kinase (SCK) values of four of these obligate carriers were found to be overlapping with that of normal values, limiting its usefulness. Since calpain levels were found to be raised in all DMD patients and obligate carriers, the estimation of calpain in all female relatives of the ones affected with DMD (with or without raised serum CK) would prove a facile index. Population screening for carrier females using this cost and labour effective index may help in assessing the carrier status and counselling the at risk families.

Adolescent↗
PubMed1998

Selenium and liver cirrhosis.

Effects of selenium deficiency, induced by thioacetamide, were investigated in rats. Thioacetamide (0.3 g/L) given in drinking water, as expected, caused a significant loss of selenium from the liver. It was accompanied by liver cirrhosis and a significant increase in the liver weight as well as liver to body weight ratio. A significant loss of selenium from spleen was also accompanied by an increase in its weight. Weights of lungs, testis and kidney, however, were not affected by thioacetamide and there was no change in their selenium content. Plasma levels of selenium were significantly reduced in the thioacetamide treated group. All these changes were confirmed to be due to selenium deficiency caused by thioacetamide, as supplementation with selenium reversed these changes. The mode of action of selenium is unknown but may involve anti-oxidant defense mechanisms.

Animals↗