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Article: Nephrotoxicity of cadmium & lead.

Gonick, H C

2008 Volume 128, Issue 4, Page(s) 335–352

Abstract: Cadmium and lead are divalent cations with a propensity to settle in the proximal tubule of the nephron, leading to nephrotoxicity. The pathophysiological results, however, tend to diverge. Cadmium in sufficient cumulative dosage leads to the production ... ...

Abstract	Cadmium and lead are divalent cations with a propensity to settle in the proximal tubule of the nephron, leading to nephrotoxicity. The pathophysiological results, however, tend to diverge. Cadmium in sufficient cumulative dosage leads to the production of the Fanconi syndrome, a generalized proximal tubular reabsorptive defect thought to be related to inhibition of both ATP production and Na-K-ATPase activity. On the other hand, lead accumulation in the proximal tubule leads to hyperuricaemia and gout, presumably by inhibiting uric acid secretion, and diminished glomerular filteration rate (GFR). Fanconi syndrome is seen unusually only in children and experimental animals. Cadmium nephrotoxicity is heralded by increased excretion of beta2-microglobulin, retinol binding protein and alpha1-microglobulin, indicative of decreased proximal tubule function. Beta2-microglobulinuria is not found in lead nephropathy. In lead nephropathy albuminuria is absent or minimal whereas in cadmium nephropathy albuminuria is variable. From the standpoint of pathology, both entities are characterized by tubulointerstitial disease and fibrosis, but only early lead nephropathy is characterized by the presence of proximal tubule nuclear inclusion bodies, due to the combination of lead with a lead binding-protein.
MeSH term(s)	Cadmium/toxicity ; Environmental Exposure ; Humans ; Kidney/drug effects ; Lead/toxicity ; Occupational Exposure
Chemical Substances	Cadmium (00BH33GNGH) ; Lead (2P299V784P)
Language	English
Publishing date	2008-10
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	390883-5
ISSN	0971-5916 ; 0019-5340
ISSN	0971-5916 ; 0019-5340
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Article: Cardiovascular effects of lead exposure.

Vaziri, N D / Gonick, H C

The Indian journal of medical research

2008 Volume 128, Issue 4, Page(s) 426–435

Abstract: Several epidemiological and clinical studies have found a link between chronic lead exposure and elevated blood pressure. In addition, a few population studies have shown possible connection between lead exposure and other cardiovascular disorders ... ...

Abstract	Several epidemiological and clinical studies have found a link between chronic lead exposure and elevated blood pressure. In addition, a few population studies have shown possible connection between lead exposure and other cardiovascular disorders including ischaemic coronary heart disease, cerebrovascular accidents, and peripheral vascular disease. The causal link between chronic lead exposure and hypertension (HTN) has been confirmed by several studies in experimental animals. In addition, the effects of lead on the heart and vascular function have been explored in a limited number of in vivo and in vitro studies. The in vivo, ex vivo and in vitro studies conducted in laboratory animal, cultured cells and isolated tissues have helped to elucidate many of the mechanisms by which lead exposure can cause HTN and cardiovascular disease. This review is intended to provide an overview of the epidemiology and the underlying mechanisms of lead-associated HTN and cardiovascular disease.
MeSH term(s)	Environmental Exposure ; Humans ; Hypertension/chemically induced ; Lead/toxicity
Chemical Substances	Lead (2P299V784P)
Language	English
Publishing date	2008-10
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	390883-5
ISSN	0971-5916 ; 0019-5340
ISSN	0971-5916 ; 0019-5340
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Article: Clinical trial of chromium and yeast supplements on carbohydrate and lipid metabolism in diabetic men.

Rabinowitz, M B / Gonick, H C / Levin, S R / Davidson, M B

Biological trace element research

2013 Volume 5, Issue 6, Page(s) 449–466

Abstract: ... triglycerides, as well as the change in plasma glucose, glucagon, and insulin or C-peptide levels in response ...

Abstract	Chromium (Cr) deficiency in experimental animals and in humans sustained by prolonged total parenteral nutrition has been shown to cause diabetes mellitus. Prior trials in humans indicated that Cr supplements, in either inorganic or organic form, may improve carbohydrate utilization. We report here a clinical double-blind, random cross-over trial of inorganic chromium trichloride, a brewer's yeast that contained Cr as glucose-tolerance-factor (GTF), a brewer's yeast extract without GTF, and a placebo. Forty-three outpatient diabetic men received three of these supplements for 4 months each. Subgroups included 21 ketosis-prone, 7 ketosis-resistant non-obese, and 15 ketosis-resistant obese men. Cr levels were followed pre- and post-treatment in hair, red blood cells, plasma, and urine. Response of carbohydrate metabolism to treatment was assessed in terms of change in insulin requirements, fasting plasma glucose, plasma cholesterol, and triglycerides, as well as the change in plasma glucose, glucagon, and insulin or C-peptide levels in response to a standard meal. In some men, these parameters were also measured after iv tolbutamide. Both the inorganic and organic oral Cr supplements increased measurable body pools of Cr in hair and red blood cells by about 25%. However, fasting plasma glucose and lipids and the glucose response to either the standard meal or to tolbutamide were not significantly altered by any of the treatments.
Language	English
Publishing date	2013-11-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/BF02988938
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Article: Is lead exposure the principal cause of essential hypertension?

Gonick, H C / Behari, J R

Medical hypotheses

2002 Volume 59, Issue 3, Page(s) 239–246

Abstract: Lead is a ubiquitous toxin, known to have adverse effects on the body even at low levels of exposure. In this review we explore whether low lead may be the principal or a major contributory cause of essential hypertension, and whether removal of lead ... ...

Abstract	Lead is a ubiquitous toxin, known to have adverse effects on the body even at low levels of exposure. In this review we explore whether low lead may be the principal or a major contributory cause of essential hypertension, and whether removal of lead from the environment may eventually reduce both the overall incidence of hypertension and the increased incidence with aging.
MeSH term(s)	Animals ; Catecholamines/physiology ; Chelating Agents/therapeutic use ; Chelation Therapy ; Environmental Exposure ; Enzyme Inhibitors/adverse effects ; Enzyme Inhibitors/pharmacology ; Ethnology ; Free Radical Scavengers/therapeutic use ; Humans ; Hypertension/chemically induced ; Hypertension/drug therapy ; Hypertension/epidemiology ; Hypertension/physiopathology ; Incidence ; Kenya/epidemiology ; Lead/adverse effects ; Lead/blood ; Lead/pharmacology ; Maximum Allowable Concentration ; Models, Biological ; Prostaglandins/physiology ; Rats ; Rats, Inbred Dahl ; Reactive Oxygen Species ; Renin-Angiotensin System/physiology ; Sodium Chloride, Dietary/adverse effects ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Sympathetic Nervous System/physiopathology ; United States/epidemiology ; Vasomotor System/drug effects ; Vasomotor System/physiopathology ; Venezuela/epidemiology
Chemical Substances	Catecholamines ; Chelating Agents ; Enzyme Inhibitors ; Free Radical Scavengers ; Prostaglandins ; Reactive Oxygen Species ; Sodium Chloride, Dietary ; Lead (2P299V784P) ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9)
Language	English
Publishing date	2002-08-16
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	193145-3
ISSN	1532-2777 ; 0306-9877
ISSN (online)	1532-2777
ISSN	0306-9877
DOI	10.1016/s0306-9877(02)00207-4
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Article: Influence of lead on rat thoracic aorta contraction and relaxation.

Shelkovnikov, S A / Gonick, H C

American journal of hypertension

2001 Volume 14, Issue 9 Pt 1, Page(s) 873–878

Abstract: Low levels of lead, but not high levels, produce hypertension. This mystery has not yet been resolved. In this study we compared the in vitro vasoresponsiveness in rat thoracic aorta to low dose (10(-8) mol/L) and high dose (10(-5) mol/L and 10(-4) mol/L) ...

Abstract	Low levels of lead, but not high levels, produce hypertension. This mystery has not yet been resolved. In this study we compared the in vitro vasoresponsiveness in rat thoracic aorta to low dose (10(-8) mol/L) and high dose (10(-5) mol/L and 10(-4) mol/L) lead acetate. In addition to the direct response to lead, we examined reactivity to norepinephrine, acetylcholine, isoproterenol, phorbol ester, and calcium in the presence and absence of lead. Neither low-dose nor high-dose lead directly affected aortic contractile or relaxant responses. However, lead, only at the highest concentration (10(-4) mol/L), increased the contractions to calcium at all submaximal calcium concentrations. We conclude that low-dose lead must increase blood pressure indirectly through a humoral effect. The reasons for the failure of high-dose lead to influence blood pressure remain to be explored.
MeSH term(s)	Acetylcholine/administration & dosage ; Animals ; Aorta, Thoracic/drug effects ; Calcium/administration & dosage ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Endothelium, Vascular/drug effects ; Female ; Hypertension/chemically induced ; Lead/administration & dosage ; Lead/adverse effects ; Male ; Models, Cardiovascular ; Myocardial Contraction/drug effects ; Norepinephrine/administration & dosage ; Phorbol Esters/administration & dosage ; Potassium Chloride/administration & dosage ; Rats ; Rats, Sprague-Dawley ; Vasoconstrictor Agents/administration & dosage ; Vasodilation/drug effects ; Vasodilator Agents/administration & dosage
Chemical Substances	Phorbol Esters ; Vasoconstrictor Agents ; Vasodilator Agents ; Lead (2P299V784P) ; Potassium Chloride (660YQ98I10) ; Acetylcholine (N9YNS0M02X) ; Calcium (SY7Q814VUP) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2001-09
Publishing country	United States
Document type	Comparative Study ; Evaluation Studies ; Journal Article
ZDB-ID	639383-4
ISSN	1879-1905 ; 0895-7061
ISSN (online)	1879-1905
ISSN	0895-7061
DOI	10.1016/s0895-7061(01)02149-5
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Article: [No title information]

Gonick, H. C.

Environmental Research, Section A

1998 Volume 76, Issue 2, Page(s) 107–113

Abstract: ... treated animals (Pb) compared to that in controls (C), returning toward normal after DMSA (105+/-2mmHg, C ... at baseline a reduced level in Pb, restored to normal by DMSA (6.6+/-1.5nmol/min/100g BW, C, vs 3.3+/-1.7, Pb ... of reactive oxygen species (ROS), was elevated at baseline in Pb, reduced by DMSA (3.6+/-0.4mymol/L, Pb, vs 1.9+/-0.2, C, and ...

Institution	8700 Beverly Blvd., USA-Los Angeles, CA 90048 c/o Harvey C. Gonick, Nephrology Section, Department of Medicine, Becker Building, Room 227, Cedars-Sinai Medical Center
Abstract	Administration of 100ppm lead acetate daily for 3 months caused hypertension in Sprague-Dawley rats, with reversal by treatment with 2,3-dimercaptosuccinic acid (DMSA) (0.5% for 2 weeks). Animals from each group were infused sequentially in 30-min intervals with saline (S), L-arginine (Arg), Arg + superoxide dismutase (SOD), S, and sodium nitroprusside (SNP). Baseline mean blood pressure (MBP) was elevated in lead-treated animals (Pb) compared to that in controls (C), returning toward normal after DMSA (105+/-2mmHg, C, vs 149+/-2, Pb, and 124+/-1, DMSA, P<0.001). Infusion of Arg caused a fall in MBP in all animals, normalizing the MBP in Pb-treated animals. SNP caused a greater fall in MBP in all groups of animals, normalizing the MBP in Pb. Measurement of urinary nitrite + nitrate (NO(x)) by chemiluminescence revealed at baseline a reduced level in Pb, restored to normal by DMSA (6.6+/-1.5nmol/min/100g BW, C, vs 3.3+/-1.7, Pb, P<0.05, vs 5.8+/-2.6, DMSA, P=NS). Infusion of arginine increased urinary NO(x) in all groups, but to a lesser degree in Pb and DMSA. Assay of plasma malondialdehyde (MDA) by HPLC, as a measure of reactive oxygen species (ROS), was elevated at baseline in Pb, reduced by DMSA (3.6+/-0.4mymol/L, Pb, vs 1.9+/-0.2, C, and 1.9+/-0.3, DMSA, P<0.01). In the Pb group, SOD resulted in a significant fall in MDA (2.0+/-0.3mymol/L, SOD, vs 3.1+/-0.1, Arg, P<0.01), but no further fall in MBP or increase in urinary NO(x). Thus, hypertension in lead-exposed animals is related to both diminished NO and increased ROS. The elevation in MBP can be ameliorated by additional NO through infusion of substrate arginine or by treatment with the ROS scavenger, DMSA. Lead-exposed animals show enhanced MBP sensitivity to the NO donors, Arg and SNP, but no further response to SOD, despite a reduction in MDA to normal. The authors speculate that lead-induced hypertension may be caused by one species of ROS which enhances vascular reactivity, and that provision of additional NO acts to scavenge the ROS and/or acts directly as a vasodilator.
Keywords	Blei ; Hypertonie ; Blutdruck ; Tierexperiment ; Stickstoffoxid ; Urin ; Messen
Language	English
Document type	Article
Database	Social Medicine (SOMED)

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Article: Summary of a symposium on natriuretic and digitalis-like factors.

Buckalew, V M / Gonick, H C

Clinical and experimental hypertension (New York, N.Y. : 1993)

1998 Volume 20, Issue 5-6, Page(s) 481–488

Abstract: An international symposium on natriuretic and digitalis-like factors was convened for the first time since 1992. Topics discussed included structures and biosynthesis of endogenous digitalis-like factors (EDLF), biologic activities, physiology function ... ...

Abstract	An international symposium on natriuretic and digitalis-like factors was convened for the first time since 1992. Topics discussed included structures and biosynthesis of endogenous digitalis-like factors (EDLF), biologic activities, physiology function and role of EDLF in hypertension, and novel natriuretic factors. Progress was reported in determining the exact structure of an isomer of ouabain isolated from bovine hypothalamus. Evidence was presented supporting the existence of a second mammalian EDLF that resembles steroids found in toads (bufodienolides). Support for endogenous synthesis of mammalian EDLF was also presented. Mammalian EDLF were reported to have effects which are different from those possessed by digitalis like steroids derived from plants. New evidence was presented implicating EDLF in various forms of hypertension in humans and animal models. Finally, several unique natriuretic factors that do not inhibit Na, K ATPase and that appear to play a role in mammalian volume regulation were discussed.
MeSH term(s)	Animals ; Cardenolides ; Cattle ; Digoxin ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/metabolism ; Humans ; Hypertension/metabolism ; Hypothalamus/chemistry ; Natriuretic Agents/physiology ; Ouabain/isolation & purification ; Saponins/chemistry ; Saponins/metabolism ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors
Chemical Substances	Cardenolides ; Enzyme Inhibitors ; Natriuretic Agents ; Saponins ; digoxin-like factors ; sodium-potassium ATPase inhibitory factor ; Ouabain (5ACL011P69) ; Digoxin (73K4184T59) ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9)
Language	English
Publishing date	1998-07
Publishing country	England
Document type	Congress
ZDB-ID	604757-9
ISSN	1064-1963 ; 0730-0077
ISSN	1064-1963 ; 0730-0077
DOI	10.3109/10641969809053226
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Zs.A 1429: Show issues

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Article: Pathophysiology of human proximal tubular transport defects.

Gonick, H C

Klinische Wochenschrift

1982 Volume 60, Issue 19, Page(s) 1201–1211

Abstract: The generalized proximal tubular transport abnormalities comprising the Fanconi syndrome (glycosuria, generalized aminoaciduria, the proximal form of renal tubular acidosis, and increased renal clearance of phosphate, urate, calcium, magnesium, and ... ...

Abstract	The generalized proximal tubular transport abnormalities comprising the Fanconi syndrome (glycosuria, generalized aminoaciduria, the proximal form of renal tubular acidosis, and increased renal clearance of phosphate, urate, calcium, magnesium, and potassium) may be ascribed to interference with "sodiumlinked" active transport. Evidence is presented that the majority of conditions known to cause Fanconi syndrome in man or experimental animals are associated with inhibitors of the renal Na-K-ATPase-ATP transport system.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Adult ; Animals ; Disease Models, Animal ; Fanconi Syndrome/drug therapy ; Fanconi Syndrome/etiology ; Fanconi Syndrome/physiopathology ; Female ; Humans ; Magnesium/therapeutic use ; Potassium/therapeutic use ; Rats ; Renal Tubular Transport, Inborn Errors/complications ; Sodium/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism ; Vitamin D/therapeutic use
Chemical Substances	Vitamin D (1406-16-2) ; Adenosine Triphosphate (8L70Q75FXE) ; Sodium (9NEZ333N27) ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9) ; Magnesium (I38ZP9992A) ; Potassium (RWP5GA015D)
Language	English
Publishing date	1982-10-01
Publishing country	Germany
Document type	Case Reports ; Journal Article ; Review
ZDB-ID	200457-4
ISSN	0023-2173
ISSN	0023-2173
DOI	10.1007/bf01716723
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Article: Lead promotes hydroxyl radical generation and lipid peroxidation in cultured aortic endothelial cells.

Ding, Y / Gonick, H C / Vaziri, N D

American journal of hypertension

2000 Volume 13, Issue 5 Pt 1, Page(s) 552–555

Abstract: ... endothelial cells were incubated in the presence of 0, 0.01, 0.1, 0.5, and 1.0 ppm lead acetate for 1, 24, and 48 h ... was measured as 2,3-dihydroxybenzoic acid (2,3 DHBA) in the cells. After exposure to lead for 48 h ...

Abstract	Early studies by our group have shown that lead-induced hypertension (HTN) is closely related to enhanced activity of reactive oxygen species (ROS). In addition, we have found indirect evidence that hydroxyl radical may be the most likely culprit in lead-exposed animals. In the present study, rat aortic endothelial cells were incubated in the presence of 0, 0.01, 0.1, 0.5, and 1.0 ppm lead acetate for 1, 24, and 48 h. At the conclusion of the incubation period cells were harvested and the media were collected. Lipid peroxidation products were measured as malondialdehyde-thiobarbituric acid (MDA-TBA) in the medium and hydroxyl radical was measured as 2,3-dihydroxybenzoic acid (2,3 DHBA) in the cells. After exposure to lead for 48 h, MDA-TBA generation and 2,3 DHBA formation were significantly increased. These data clearly demonstrate that lead exposure promotes hydroxyl radical generation and induces oxidative stress in isolated endothelial cells, mimicking the effects observed in lead-exposed animals. Enhanced inactivation of endothelium-derived nitric oxide by locally produced oxygen free radicals could contribute to endothelial dysfunction and HTN in lead-exposed animals.
MeSH term(s)	Animals ; Aorta, Thoracic/drug effects ; Aorta, Thoracic/metabolism ; Aorta, Thoracic/pathology ; Cell Count ; Cell Survival/drug effects ; Cells, Cultured ; Culture Media/chemistry ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Hydroxybenzoates/metabolism ; Hydroxyl Radical/metabolism ; Hypertension/chemically induced ; Hypertension/metabolism ; Hypertension/pathology ; Lead/toxicity ; Lipid Peroxidation/drug effects ; Lipid Peroxidation/physiology ; Malondialdehyde/metabolism ; Rats ; Rats, Sprague-Dawley ; Thiobarbiturates/metabolism
Chemical Substances	Culture Media ; Hydroxybenzoates ; Thiobarbiturates ; Lead (2P299V784P) ; Hydroxyl Radical (3352-57-6) ; Malondialdehyde (4Y8F71G49Q) ; 2,3-dihydroxybenzoic acid (70D5FBB392) ; thiobarbituric acid (M1YZW5SS7C)
Language	English
Publishing date	2000-05
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	639383-4
ISSN	1879-1905 ; 0895-7061
ISSN (online)	1879-1905
ISSN	0895-7061
DOI	10.1016/s0895-7061(99)00226-5
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Article: Kidney in patients with abnormalities in uric acid metabolism.

Gonick, H C

Contributions to nephrology

1977 Volume 7, Page(s) 79–96

MeSH term(s)	Acute Disease ; Aged ; Animals ; Dogs ; Female ; Gout/complications ; Gout/metabolism ; Gout/pathology ; Humans ; Kidney/physiopathology ; Kidney Calculi/metabolism ; Kidney Diseases/etiology ; Kidney Diseases/metabolism ; Kidney Diseases/pathology ; Rats ; Uric Acid/blood ; Uric Acid/metabolism ; Uric Acid/urine
Chemical Substances	Uric Acid (268B43MJ25)
Language	English
Publishing date	1977
Publishing country	Switzerland
Document type	Journal Article
ISSN	0302-5144
ISSN	0302-5144
DOI	10.1159/000400117
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