Effects of lead on collagen synthesis and renal function in the rat

Rodolfo-Sioson, Sonya Agnesi

doi:10.31274/rtd-180813-4930

Cited by 2 publications

(3 citation statements)

References 235 publications

(245 reference statements)

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“…These results indicate that acute low-level lead treatment has significant effects on the regulation of collagen genes as a group in astrocytes. Leadinduced alteration of collagen biosynthesis in astrocytes has potential implications for the effects of lead on the blood-brain barrier as suggested by previous studies (Rodolfo-Sioson and Ahrens, 1980). Effects of lead on collagen biosynthesis have also been studied in relation to rheumatoid arthritis (Goldberg et al, 1983), skeletal abnormalities (Pounds et al, 1991;Klein and Wiren, 1993;Hicks et al, 1996), and lead-based skin ointments (Vandeputte et al, 1990).…”

Section: Angiogenesis and Blood-brain Barrier-related Genesmentioning

confidence: 84%

“…Lead also binds to collagen (Miksik et al, 1999). Previous studies have demonstrated lead-induced alterations in collagen biosynthesis at both the mRNA and protein level in vitro (Vistica et al, 1977;Goldberg et al, 1983;Long and Rosen, 1992;Klein and Wiren, 1993;Hicks et al, 1996) and in vivo (Rodolfo-Sisoson and Ahrens, 1980;Rana and Prakash, 1986;Ahrens, 1993). The effects of lead on collagen biosynthesis have been linked to calcium-dependent signaling pathways that include PKC and EGF (Pounds et al, 1991;Long and Rosen, 1992).…”

Section: Angiogenesis and Blood-brain Barrier-related Genesmentioning

confidence: 95%

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Microarray Analysis of Differential Gene Expression in Lead-Exposed Astrocytes

Bouton

Hossain

Frelin

et al. 2001

Toxicology and Applied Pharmacology

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Section: Angiogenesis and Blood-brain Barrier-related Genesmentioning

confidence: 84%

Section: Angiogenesis and Blood-brain Barrier-related Genesmentioning

confidence: 95%

Microarray Analysis of Differential Gene Expression in Lead-Exposed Astrocytes

Bouton

Hossain

Frelin

et al. 2001

Toxicology and Applied Pharmacology

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“…The most direct evidence is the early work by Hass and co-workers who reported an inhibitor effect of lead on vitamin D-stimulated matrix production in bone and arteries in the rabbit (20). The inhibition of collagen synthesis by lead has been confirmed by subsequent investigations using human synovial cells, cultured embryonic chick bone, skin, or cultured mouse fibroblasts (56)(57)(58)(59). Again, the dose-response relationships and clinical significance remain to be established.…”

Section: Collagenmentioning

confidence: 91%

Cellular and molecular toxicity of lead in bone.

Pounds

Long

Rosen

1991

Environ Health Perspect

291

131

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To fully understand the significance of bone as a target tissue of lead toxicity, as well as a reservoir of systemic lead, it is necessary to define the effects of lead on the cellular components of bone. Skeletal development and the regulation of skeletal mass are ultimately determined by the four different types of cells: osteoblasts, lining cells, osteoclasts, and osteocytes. These cells, which line and penetrate the mineralized matrix, are responsible for matrix formation, mineralization, and bone resorption, under the control of both systemic and local factors. Systemic components of regulation include parathyroid hormone, 1,25-dihydroxyvitamin D3, and calcitonin: local regulators include numerous cytokines and growth factors. Lead intoxication directly and indirectly alters many aspects of bone cell function. First, lead may indirectly alter bone cell function through changes in the circulating levels of those hormones, particularly 1,25-dihydroxyvitamin D3, which modulate bone cell function. These hormonal changes have been well established in clinical studies, although the functional significance remains to be established. Second, lead may directly alter bone cell function by perturbing the ability of bone cells to respond to hormonal regulation. For example, the 1,25-dihydroxyvitamin D3-stimulated synthesis of osteocalcin, a calcium-binding protein synthesized by osteoblastic bone cells, is inhibited by low levels of lead. Impaired osteocalcin production may inhibit new bone formation, as well as the functional coupling of osteoblasts and osteoclasts. Third, lead may impair the ability of cells to synthesize or secrete other components of the bone matrix, such as collagen or bone sialoproteins (osteopontin). Finally, lead may directly effect or substitute for calcium in the active sites of the calcium messenger system, resulting in loss of physiological regulation. The effects of lead on the recruitment and differentiation of bone cells remains to be established. Compartmental analysis indicates that the kinetic distribution and behavior of intracellular lead in osteoblasts and osteoclasts is similar to several other cell types. Many of the toxic effects of lead on bone cell function may be produced by perturbation of the calcium and cAMP messenger systems in these cells.

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Effects of lead on collagen synthesis and renal function in the rat

Cited by 2 publications

References 235 publications

Microarray Analysis of Differential Gene Expression in Lead-Exposed Astrocytes

Microarray Analysis of Differential Gene Expression in Lead-Exposed Astrocytes

Cellular and molecular toxicity of lead in bone.

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