Chronic lead poisoning magnifies bone detrimental effects in an ovariectomized rat model of postmenopausal osteoporosis

Lee, Ching Ming; Terrizzi, Antonela Romina; Bozzini, Clarisa; Piñeiro, Adriana; Conti, Maria; Martínez, María Pilar

doi:10.1016/j.etp.2015.09.007

Cited by 14 publications

(3 citation statements)

References 12 publications

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“…Lead integrates into hydroxyapatite and can be stored for many years in bone 9 , leaching back into the body even after exposures are eliminated 10,11 and thus taking years or decades to be fully cleared from the body. Deposition of lead in the bone also interferes with bone cell signaling, maturation, and differentiation [12][13][14] , leading to impaired fracture healing 15 and increased risk of osteoporosis 16,17 .…”

Section: Introductionmentioning

confidence: 99%

Nucleic Acid Aptamers Protect Against Lead (Pb(II)) Toxicity

Anwar,

De Ayreflor Reyes,

John

et al. 2024

Preprint

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Lead (Pb(II)) is a pervasive heavy metal toxin with many well-established negative effects on human health. Lead toxicity arises from cumulative, repeated environmental exposures. Thus, prophylactic strategies to protect against the bioaccumulation of lead could reduce lead-associated human pathologies. Here we show that DNA and RNA aptamers protect C. elegans from toxic phenotypes caused by lead. Reproductive toxicity, as measured by brood size assays, is prevented by co-feeding of animals with DNA or RNA aptamers. Similarly, lead-induced behavioral anomalies are also normalized by aptamer feeding. Further, cultured human HEK293 and primary murine osteoblasts are protected from lead toxicity by transfection with DNA aptamers. The osteogenic development, which is decreased by lead exposure, is maintained by prior transfection of lead-binding DNA aptamers. Aptamers may be an effective strategy for the protection of human health in the face of increasing environmental toxicants.

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Section: Introductionmentioning

confidence: 99%

Nucleic Acid Aptamers Protect Against Lead (Pb(II)) Toxicity

Anwar,

De Ayreflor Reyes,

John

et al. 2024

Preprint

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“…Most of the population must have lead in their organisms due to occupational or environmental exposure [ 1 – 3 ]. A variety of harmful effects may arise from lead intoxication, which include alterations in bone density [ 4 , 5 ] and cognitive [ 6 , 7 ] and cardiovascular disorders, such as hypertension [ 8 , 9 ], and these adverse effects may result from both duration of exposure and blood lead levels [ 10 ]. The National Institute for Occupational Safety and Health, USA, stated that reference blood lead levels for adults should be ≥5 μ g/dL [ 11 ] and lead-induced hypertension has been shown in experimental animals with low blood lead levels (9–37 μ g/dL) [ 9 , 12 – 14 ].…”

Section: Introductionmentioning

confidence: 99%

Clinical and Experimental Evidences of Hydrogen Sulfide Involvement in Lead-Induced Hypertension

Possomato-Vieira

Gonçalves-Rizzi

Nascimento

et al. 2018

BioMed Research International

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Lead- (Pb-) induced hypertension has been shown in humans and experimental animals and cardiovascular effects of hydrogen sulfide (H2S) have been reported previously. However, no studies examined involvement of H2S in Pb-induced hypertension. We found increases in diastolic blood pressure and mean blood pressure in Pb-intoxicated humans followed by diminished H2S plasmatic levels. In order to expand our findings, male Wistar rats were divided into four groups: Saline, Pb, NaHS, and Pb + NaHS. Pb-intoxicated animals received intraperitoneally (i.p.) 1st dose of 8 μg/100 g of Pb acetate and subsequent doses of 0.1 μg/100 g for seven days and sodium hydrosulfide- (NaHS-) treated animals received i.p. NaHS injections (50 μmol/kg/twice daily) for seven days. NaHS treatment blunted increases in systolic blood pressure, increased H2S plasmatic levels, and diminished whole-blood lead levels. Treatment with NaHS in Pb-induced hypertension seems to induce a protective role in rat aorta which is dependent on endothelium and seems to promote non-NO-mediated relaxation. Pb-intoxication increased oxidative stress in rats, while treatment with NaHS blunted increases in plasmatic MDA levels and increased antioxidant status of plasma. Therefore, H2S pathway may be involved in Pb-induced hypertension and treatment with NaHS exerts antihypertensive effect, promotes non-NO-mediated relaxation, and decreases oxidative stress in rats with Pb-induced hypertension.

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“…In addition, it is well known that bone is an organ system that predominantly stores Pb (accumulating with age, only 70% of total Pb body burden in children but approximately 90% in adults; EFSA, 2010). Laboratory animal and human studies have found associations between chronic Pb exposure and bone damage, including reduced BMD (Campbell & Auinger, 2007;Lee et al, 2016;Theppeang et al, 2008), impaired bone structures (Wong et al, 2015) and even increased risk of osteoporosis (Sun et al, 2008).…”

mentioning

confidence: 99%

Co‐exposure of cadmium and lead on bone health in a southwestern Chinese population aged 40‐75 years

Yan

et al. 2019

J of Applied Toxicology

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Both cadmium (Cd) and lead (Pb) are associated with bone health, but studies exploring the effects of Cd and Pb co‐exposure on bone health are rare. This study aimed to assess the interactive effects of Cd and Pb co‐exposure on bone health. In total, 799 participants, living in the targeted areas (located in southwestern China) for more than 15 years, aged 40‐75 years, and subsisted on homegrown rice and vegetables were investigated. Cd and Pb levels in urine and blood samples, as well as bone mineral density, T‐ and Z‐score were determined. After being adjusted for covariates, the T‐score was negatively correlated with blood Pb in men (P < .05); for women and non‐smoking women, the T‐score was negatively correlated with urinary Pb (P < .05). Moreover, after being adjusted for covariates, the Z‐score was negatively correlated with urinary Pb in non‐smoking women (P < .05). No positive association of prevalence of osteoporosis with Cd and Pb exposure was found. However, at an additive scale, positive interactions of urinary Cd and Pb on the prevalence of osteoporosis for women and non‐smoking women, and the same interactions to blood Cd and Pb for men were found. There was also a positive interaction of urinary Cd and Pb for women at a multiplicative scale. This study suggests Cd and Pb exposure could exert detrimental effects on bone health, with possible underlying interactions. Nevertheless, more studies are needed to explore the interactive effects of heavy metal co‐exposure.

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Chronic lead poisoning magnifies bone detrimental effects in an ovariectomized rat model of postmenopausal osteoporosis

Cited by 14 publications

References 12 publications

Nucleic Acid Aptamers Protect Against Lead (Pb(II)) Toxicity

Nucleic Acid Aptamers Protect Against Lead (Pb(II)) Toxicity

Clinical and Experimental Evidences of Hydrogen Sulfide Involvement in Lead-Induced Hypertension

Co‐exposure of cadmium and lead on bone health in a southwestern Chinese population aged 40‐75 years

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